Schwarzenberger - Skin Intro Flashcards
1
Q
What are some important factors in the skin PE?
A
- Use all available clues -> look at the patient first, then look at the skin
- Complete skin exam: good lighting and a naked patient (incl: skin, hair, nails, mucous membranes)
- Identify the lesion type and note any modifying factors (color, size, number)
- Describe the distribution and pattern: generalized, localized to, linear, grouped
2
Q
What is this?
A
- Papule: palpable lesion elevated above skin surface
- <0.5 cm in diameter
- Do not have to be perfectly round
- Can also be umbilicated
3
Q
What is this?
A
- Nodule: firm (indurated) lesion thicker or deeper than 0.5cm
- Cyst would be even bigger
4
Q
What is this?
A
- Macule: flat, non-palpable lesion <0.5cm in diameter
- Patch if >0.5 cm
5
Q
What is the main role of the epidermis? Dermis?
A
- Epidermis: Barrier (protection)
- Dermis: Structural and nutritional support
6
Q
What is this?
A
- Plaque: palpable lesion elevated above skin surface >0.5cm (classic example is psoriasis)
7
Q
What are these?
A
- Vesicles: blister <0.5 cm
- Herpes: multiple, coalescing vesicles in a herpetiform distribution -> see attached image
- Bullae are bigger
- Pustule if it has white/yellow fluid in it
8
Q
Can Staph infect the skin?
A
- Not unless you have a scratch or surgically cut the skin
- Can infect the hair follicles
9
Q
What is this?
A
- Wheal = hive: temporary raised areas of the skin surrounded by a red base
10
Q
What is this?
A
- Spider angiomas: capillary malformations
11
Q
What is this?
A
- Lichenification: result of repetitive scratching
- Granular layer becomes thickened (hyperkeratotic)
12
Q
What are these?
A
- Excoriations -> much more superficial than ulcers, which extend down into the subcu tissue (see attached)
13
Q
What is this?
A
- Atrophy: cigarette/tissue paper wrinkling
- Epidermis can virtually be holding on by blood vessels, and can sometimes get ecchymoses quite easily
14
Q
What are the important functions of the skin?
A
- Barrier function
- Immune recognition and surveillance: by antigen presenting cells (Langerhans cells in epidermis; lymphocytes and dermal dendritic cells in dermis)
- Damage repair: keratinocytes proliferate in epidermis in response to injury or inflammation, fibroblasts in dermis
- Thermoregulation: vasculature in the dermis
- Protection from UV radiation: malanocytes
- Communication
- Failure at any level can result in damage/disease
15
Q
How does the skin function as a barrier? What can happen if it is defective (4)?
A
- Physical barrier, regulating water loss, protecting against mechanical, chemical and microbial insults from outside world
- Possible consequences of defective skin barrier:
1. Dehydration
2. Infection
3. Injury of skin, such as ulcers
4. Inflammation - Example: atopic dermatitis (eczema) due to mutation in fillagrin gene (see attached image)
16
Q
What condition is this? Associated mutation?
A
- Atopic dermatitis (eczema)
- Fillagrin gene mutations
17
Q
Why is skin a poor host for growth of orgs?
A
- Intact skin is poor host for growth of organisms:
1. Dry
2. Impermeable
3. Sheds off
4. No blood vessels in the epidermis - Both innate AND adaptive immunologic processes important in skin
18
Q
What can happen if skin immune regulation is compromised?
A
- Consequences of impaired skin immune function include:
1. Infection
2. Skin cancer
3. Inflam and/or autoimmune skin diseases
4. Allergic reactions - Skin can be involved/injured, either primarily or secondarily (“innocent bystander”) by immunologic functions
19
Q
What condition is this?
A
- Bullous pemphigoid: auto-antibodies to hemidesmosomes (adhesion molecule)
- IF: frozen skin overlayed with fluorescently labeled Ab’s
20
Q
What conditions is this?
A
- Pemphigus vulgaris: auto-Ab’s to desmosomes
- More erosions than blisters
- Chicken-wire IF
21
Q
How does this happen?
A
- Neuropathic ulcers: people with diabetes are more prone to pressure ulcers because they don’t “feel” that they need to move around
- Trigeminal trophic syndrome: trigeminal N loss of sensation, leading to scratching (can’t feel the pain they are inducing)
22
Q
How is the skin involved in photoprotection?
A
- Epidermis contains melanin, which helps protect against damage from ultraviolet radiation
1. UV light can also damage the immune system - Genetic and/or acquired conditions can reduce or eliminate pigment in skin
- Loss of photoprotection increases risk of burning and skin cancer
23
Q
What are the acute effects of UV radiation on skin?
A
- Inflammation (sunburn)
- Immunomodulation: can even cause chills, headaches
- Epidermal hyperplasia
- Vitamin D photosynthesis
- DNA damage: apoptosis or cell cycle arrest to repair
24
Q
What are the chronic effects of UV radiation?
A
- Photoaging: sun is really what ages the skin (more so than just age)
- Photocarcinogenesis:
1. Basal cell and squamous cell carcinomas
2. Melanoma
a. Lifetime incidence of melanoma has gone from 1 in 3500 to 1 in 50
b. AA more likely to get melanoma on hands and feet
25
Q
What histo changes do we see w/chronic UV radiation?
A
- Solar elastosis: elastin fibers that have been damaged by UV radiation, and are broken and clumped
- Collagen is what keeps your skin young
26
Q
What is xeroderma pigmentosum?
A
- Failure in the DNA repair process -> start getting skin cancers before they are 10 years old
27
Q
What is hypohidrotic ectodermal dysplasia?
A
- Genetic condition due to mutations in EDAR (“Ectodyplasin A receptor”) gene: can’t sweat, so they overheat easily bc they can’t regulate temp
1. Protein critical for proper interaction between developing ectoderm and mesoderm - Results in abnormal hair follicles, sweat glands, and teeth
28
Q
What pathologic process causes this?
A
- Small vessel vasculitis
- Diseases that injure blood vessels disrupt circulation, resulting in cutaneous necrosis and/or ulceration
1. Antiphospholipid Ab syndrome can cause widespread cutaneous necrosis (see attached image)
29
Q
What types of symptoms can disorders of nerve sensation in the skin cause?
A
- Itch
- Dysesthetic pain/burning (postherpetic neuralgia: nerve pain caused by varicella zoster virus)
- Hyperesthesia: excessive sensitivity
- Loss of sensation can also result in insensitivity to injury (think: diabetic peripheral neuropathy)
30
Q
Friendly reminder.
A
Good job!
31
Q
What are the 3 layers of the skin, and their cells?
A
-
Epidermis: Keratinocytes (>90%)
1. Melanocytes, Langerhans, Merkel cells (light touch sensory cells; can cause lethal cancers) -
Dermis: Fibroblasts, collagen, elastic
1. Blood vessels, nerve endings: if you scrape knee and it bleeds, you’re in the dermis - Subcutis: Fat, blood vessels, fibrous septae (cause cellulite)
32
Q
What is this?
A
- Normal skin
- Blood vessels go up into the dermal papillae: this is why you can get “needle-point bleeds” when you get a scrape
33
Q
What are the main functions of the epidermis vs. the dermis and subcutis?
A
- Epidermis: primarily a barrier function, protection, and wound healing (must be able to “fix itself”)
- Dermis/subcutis: structural and vascular support and innervation
34
Q
How often does the epidermis regenerate? How does this happen?
A
- Epidermis is a self-renewing tissue that “sheds” itself on average every 28+ days
1. 14 days to reach stratum corneum
2. 14 days to desquamate
3. This happens a lot faster in psoriasis as a result of inflammation - Keratinocytes grow from stem cells in the basal layer and are shed from the surface -> terminally differentiate as they move upwards
- Apoptosis (“programmed cell death”) normally low in epidermis, but can increase in some situations
35
Q
What are the four layers of the epidermis?
A
- Organized based on position and structural properties of keratinocytes:
1. Stratum corneum
2. Stratum granulosum: granular cell layer
3. Stratum spinosum: spiny layer
4. Stratum basale: source of stem cells (division starts here)
a. Adhere to dermis (BM zone) through hemidesmosomes
36
Q
What are the 4 major types of cell junctions?
A
- Desmosomes: KC-KC adhesion
- Hemidesmosomes: epidermis-dermis adhesion
- Adherens junctions: links actin filaments KC-KC
- Gap junctions: connexin proteins, important in cell-cell communication
37
Q
What layer of the epidermis is this? What happens here?
A
- Spinous layer: cells stop dividing and start terminal differentiation
- Develop lipids (lamellar granules) important in barrier function
- “Spiny” due to visible desmosomes with which one KC adheres to another
38
Q
What layer of the epidermis is this? What happens here?
A
- Stratum granulosum: IC keratohyaline granules synthesized (including profilaggrin)
- Lipids in lamellar granules secreted into IC space to form water barrier to keep water in skin
39
Q
What layer of the epidermis is this? What happens here?
A
- Stratum corneum: nuclei, organelles degenerate, and cells flatten
- Profilaggrin processed into filaggrin, which help keep water in cells
- Keratins (structural cytoskeletal proteins) combine with filaggrin into macrofibrils that create protective layer
40
Q
What are keratins?
A
- Major fibrous structural proteins in hair and nails; >40 different kinds
- Combine to form intermediate filaments (KNOW THIS)
- Pairs differ by location in body
- Mechanically stabilize cell against physical stress
- Have lg amounts of sulfur-containing amino acid cysteine (esp. hair and nails -> this is why there is a sulfur-y smell when you burn your hair)
41
Q
What kinds of filaments to keratins combine to form?
A
INTERMEDIATE
42
Q
What 2 sites are these histo pics from?
A
- Note the stratum corneum differences
1. Trunk on the left: basket-weave, loose
2. Palm on the right: more protective, dense
43
Q
Why is stratum corneum described as “brick and mortar?”
A
- Bricks: flattened keratinocytes filled with keratin and filaggrin
- Mortar: lipid mixture surrounding keratinocytes, providing water barrier
44
Q
What type of cell is this? What does it do?
A
- Melanocyte: pigment-producing dendritic cells
- Derived from neural crest; migrate in embryonic development
1. Defect in neural crest migration can lead to melanoma in unsuspected places - “Live” along basal cells, w/about one per 10 keratinocytes (see attached image)
- Produce melanin, a radiation-absorbing pigment, and transfer it to surrounding keratinocytes via dendritic processes
- Primary defense against ultraviolet radiation
45
Q
Appreciate this melanocyte-keratinocyte unit
A
Good job!
46
Q
What are these? What do they do?
A
- Langerhans cells: dendritic cells in mid-epidermis
- One of major immunologic players in skin
- Recognize abnormal Ag’s in skin; take up, process, and present to lymphos in regional lymph nodes
1. Migratory: move to lymph tissue to present (processing and presentation) - Important in allergic reactions, tumor surveillance
47
Q
What are Merkel cells?
A
- Epidermal cells
- Associated with light touch sensation
- Can develop into malignant tumors (rare, but lethal)
48
Q
How thick is the dermis? What is in it?
A
- Thickness varies significantly by site: 1-4 mm thick, and functions primarily as a support layer
- Contains: blood vessels and lymphatics, nerves, sweat and oil glands, and hair follicles
- Note: sebaceous glands follow hair follicles, but eccrine do NOT
49
Q
What do fibroblasts do in the dermis?
A
- 1o cell in the dermis (mesenchymal origin)
- Responsible for synthesis and degradation of CT proteins, incl collagen, elastin, glycosaminoglycans and other glycoproteins
- Injury to skin triggers fibroblast mitosis
- Responsible for wound healing and scar formation
50
Q
What are these?
A
- Mast cells: specialized tissue cells rich in histamine and heparin granules
- Release granules when triggered by injury or binding of IgE antibodies during allergic reactions
- Histamine and other mediators important in allergic reactions and wound healing (this is why healing scars can be itchy)
1. Cause characteristic “wheal and flare”
51
Q
What is this? What does it consist of?
A
- Pilosebaceous (hair/oil) unit:
1. Hair follicle (extend through dermis into subcutis)
2. Sebaceous (oil) gland
3. Apocrine sweat glands (in axilla and anogenital skin)
4. Arrector pili muscle (goose bumps)
52
Q
What are eccrine sweat glands?
A
- “True” sweat glands; present throughout the body
- Open directly onto the skin (not associated with hair follicle)
- Function to regulate temperature by evaporative cooling of sweat
53
Q
What is the subcutis?
A
- Fat layer that separates dermis from underlying structures including fascia, muscle, organs
- Subcutis provides:
1. Insulation
2. A source of energy
3. Protection from injury
54
Q
What is up with these cells?
A
-
Sun-burn cells: damaged keratinocytes -> apoptosis is normal response to sun-damaged cells
1. Failure to “delete” damaged cells can result in skin cancer
2. Sunburn = INC apoptosis
55
Q
What is this?
A
- Epidermolysis Bullosa Simplex: genetic mutations in Keratin 5/14 (so no cure)
- Bullae arising on the toes ( A ) and the plantar surface ( A,B ) at sites of lateral or rotary traction
- Keratinocytes can split in half -> can go unrecognized for long periods of time
56
Q
What is this?
A
- Melanoma: growth of malignant (cancerous) melanocytes
- ASYMMETRY -> melanomas (grossly and histologically)
- A nevus (mole) would be a benign collection of melanocytes
57
Q
What is this?
A
- Erythema nodosa
- Affects the subcutis
58
Q
Probably should know these.
A
Good job!
