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Patho > Disease of Skin > Flashcards

Disease of Skin Flashcards

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
Q

3-10mm bruise

A

Purpura

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26
Q

A bruise that arise from small vessels

A

Petechiae

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27
Q

Burns

A

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
Q

3rd degree burns

what to expect

A
  • 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
Q

The Rule of 9’s

A

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
Q

Surface hyperemia

A

Sun burns basically

31
Q

Third-Degree Burn Scars

A

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
Q

Hypothermia/Frostbite

A
  • Frostnip (red)
  • Superficial frostbite (gets whitish blister/pimple)
  • Deep frostbite (turn dark and black)
33
Q

Skin Infections

A

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
Q

Skin Infections Types

A

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
Q

Verruca (Warts)

A

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
Q

Herpes Simplex Type I

A

Cold sore
- Very Infectious
- Self limiting

37
Q

Herpes zoster

A

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
Q

Impetigo

A

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
Q

Persistent impetigo may
lead to

A

immune-complex
GN

40
Q

Tinea Cruris

A

Skin Fungus; near genital, inner thighs, and buttocks
- itchy, red, often ring-shaped rash in the groin area.

41
Q

Tinea Corporis

A

Ringworm of the body; rash caused by fun
- t’s usually an itchy, circular rash with clearer skin in the middle

42
Q

Tinea Capitis

A

Ringworm of the scalp
- Is a skin disorder that affects children almost exclusively
- Itching, scaly, inflammed balding
- Persistent and very contagious.

43
Q

Candidiasis

A

Diaper Rash (not changed regularly)
- Fungal infection caused by a yeast (a type of fungus) called Candida

44
Q

Fungal Infection of IV Catheter Site

A

Looks very very clear. God it’s stuck in my brain now

45
Q

Scabiese

A
  • intense itching and a pimple-like skin rash.
  • Show up in the flectur point
46
Q

Brown Recluse (Loxosceles reclusa)

A

Venom of a brown recluse can cause a severe lesion by destroying skin tissue (skin necrosis)
- There is no antivenom for it

46
Q

Brown Recluse (Loxosceles reclusa)

A

Venom of a brown recluse can cause a severe lesion by destroying skin tissue (skin necrosis)
- There is no antivenom for it

47
Q

Allergic Dermatitis & Hypersensitivity

A
  • 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
Q

Allergic Contact Dermatitis

A

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
Q

Cross Sensitization

A

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
Q

Dermatographia

A

A condition in which lightly scratching your skin causes raised, red lines where you’ve scratched.

51
Q

Cyanosis

A

bluish color in the skin, lips, and nail beds caused by a shortage of oxygen in the blood

52
Q

Carbon Monoxide Poisoning

A

skin is cherry red

53
Q

If any sliver metal goes to the dermis

A

gonna result in argyria; which is discolorlation
- Will not go away

54
Q

Neoplasia and Tumor-like Conditions

A

Benign
- Warts
- Seborrheic keratosis
- Nevi
- Angioma

Malignant
- Basal cell carcinoma
- Squamous cell carcinoma
- Malignant melanoma
- Angiosarcoma
- Lymphoma

55
Q

Congenital Nevi

A

Will stay benign; Change in the pigment of skin (discoloration of some areas)

56
Q

Solar Keratosis

Also called ‘actinic keratosis’

A

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
Q

Basal Cell Carcinoma

most common malignancy worldwide

A

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
Q

Squamous Cell Carcinoma

A

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
Q

Malignant Melanocarcinoma

A

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
Q

Malignant Melanocarcinoma

Prognosis

A

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
Q

Malignant Melanocarcinoma

Arises from?

A

Arises from melanocytes (neural crest cells) either de novo or from premalignant condition. Can have in situ stage

62
Q

Melanoma Risk Factors

A
  • 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
Q

Recognizing Malignant Melanoma

A
  • Change in size
  • Change in color
  • Change in shape
  • Increase in elevation
  • Change in surface
  • Change in surrounding skin
  • Bleeding
  • Change in texture
64
Q

Malignant Melanoma Survival

A

Level 1: will survive
Level II: 75% survival
Level III 50% survival
Level IV and V: 10% survival

Patho (17 decks)

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