Tutorial 1- Skin Basics Flashcards
1
Q
Macules
A
flat, less than 1cm lesion that is not raised or thickened.
Ex. Freckles, ash Leaf macule In tuberous Sclerosis
2
Q
papules
A
elevated, less than 1cm lesion. Surface of lesion may be rounded, flat, or scaly
ex. molluscum contagiosum
3
Q
patches
A
flat, greater than 1cm lesion that is not thickened, depressed, or indurated
Examples: nevus flammeus (port wine stain), Nevus of Ota, and patch stage mycosis fungoides
4
Q
plaques
A
elevated, greater than 1cm skin lesion
Examples: eroded plaque in mycosis fungoides, and the scaly, salmon-colored lichenified plaques in psoriasis vulgaris
5
Q
nodules
A
Solid, elevated lesion >1cm involving epidermis, dermis and subcutis (subcutaneous) or subcutis alone.
Examples: keratoacanthoma type squamous cell carcinoma, subcutaneous nodules from metastasis of a distant visceral malignancy
6
Q
pustules
A
a papule which contains a collection of purulent exudate
Examples: staph infection, herpes and pustular psoriasis
7
Q
vesicles
A
fluid-filled lesions less than 1cm in diameter
Examples: Rhus dermatitis (poison ivy) and bullous pemphigoid
8
Q
bullae
A
fluid-filled lesions greater than 1cm in diameter
Examples: Rhus dermatitis (poison ivy) and bullous pemphigoid
9
Q
lichenification
A
chronic thickening of the skin, with accentuation of skin lines
Plaques are often described as lichenified.
Examples of lichenified lesions include chronic plaque psoriasis, lichen simplex chronicus, chronic eczema, and other chronic dermatitis.
10
Q
crusts
A
thick, adherent dried serum, blood, or purulent exudate
Examples: impetigo, crusted cutaneous herpes, and surgical wounds with suboptimal wound care
11
Q
scales
A
thickened, loose fragments of stratum corneum. Scale may be confluent, thick, and micaceous, as seen in psoriasis vulgaris. Alternatively, fine scale may be seen in tinea.
Example: Fine scale overlying hypopigmented macules and patches of tinea versicolor
12
Q
erosions
A
a partial focal loss of epidermis. Heals without scarring.
Examples: denuded blisters of pemphigus and staphylococcal scalded skin syndrome, and widespread pemphigus foliaceus
13
Q
ulcerations
A
full-thickness focal loss of epidermis and underlying dermis. Heals with scarring.
Examples: venous stasis ulcers, pyoderma gangrenosum, and ulcers from chronic infections.
14
Q
eruptions
A
rash
15
Q
morbilliforms
A
rash that looks like measles. The rash consists of macular lesions that are red and usually 2–10 mm in diameter
16
Q
Telangiectasias
A
fine blood vessels
17
Q
Excoriations
A
Skin abrasions, usually superficial, due to scratching of the skin.
These lesions may be the result of scratching with fingernails or other objects leading to linear breaks in the skin. The scratching is often secondary to pruritus. Patients presenting with excoriations may have a wide variety of disorders including scabies, atopic dermatitis, and neurotic excoriations produced by habitual picking with the fingernails.
18
Q
Comedones
A
Skin-coloured, small bumps (papules) frequently found on the forehead and chin of those with acne. A single lesion is a comedo. Open comedones are blackheads; black because of surface pigment (melanin), rather than dirt. Closed comedones are whiteheads; the follicle is completely blocked
19
Q
Urticaria
A
hives/welts
20
Q
Atrophy
A
thinning of the skin
21
Q
Functions of the Skin (6):
A
Containment Protection Healing after injury Sensation Thermoregulation Communication
22
Q
The 4 Layers of the Epidermis
A
- Stratum corneum
- Stratum granulosum (granular cell layer)
- Stratum spinosum (spiny layer, prickle layer)
- Stratum basale (basal layer)
23
Q
Primary Cell Type of the Epidermis
A
The keratinocyte.
Keratinocytes become increasingly differentiated as they move from the basal layer to the spiny layer, granular layer, and finally the stratum corneum.
24
Q
What layer is the stem cell layer?
A
Stratum basale
25
What kinds of Keratin are found in high concentration in the Stratum Basale?
keratin 5 and keratin 14
26
What layer do desmosomes start?
| What is a clinical correlation?
Stratum spinosum
Clinical Correlation: Pemphigus Vulgaris is autoimmune destruction of desmosomes between keratinocytes. Due to IgG antibody against desmoglein (type II hypersensitivity. It presents as skin and oral mucosa bullae
27
Why is the stratum granulosum called the granular layer
Because of the high density of keratohyaline granules within the cytoplasm of these cells
28
What types of keratin are found in high concentration in the upper layers of the epidermis
keratin 1 and keratin 10
29
What are the cells of the stratum corneum composed of?
The cells are flat and comprised of keratin filaments and keratohyalin granules which link these filaments.
Note: Keratinocytes in the stratum corneum lack a nucleus and organelles.
30
What is X-linked ichthyosis (XLI)?
Caused by a genetic defect in the steroid sulfatase gene. This causes abnormalities in the processing of keratinocyte cholesterol molecules which are needed for the proper formation of the stratum corneum. XLI patients have an unusually thick stratum corneum which does not provide normal barrier function.
Clinical presentation: dark plate-like scales throughout the entire trunk and extremities with sparing of the face, palms and soles, and flexural skin
31
What are melanocytes?
Melanocytes are melanin-containing pigment cells located in the basal layer.
32
Where are melaoncytes derived from?
The neural crest
33
What do melanocytes do?
transfer pigmented melanosomes to nearby keratinocytes.
34
What determines skin color?
It is the quantity and quality of melanin, not the density of melanocytes, which determines skin color. The melanosomes of darkly pigmented skin contain more melanin and are larger in diameter than the melanosomes of lighter skin.
35
What is vitiligo?
Vitiligo is a relatively common skin condition, affecting 0.5-2.0% of the world population. The disease is characterized by amelanotic macules and patches.
36
What is the pathogenesis of vitiligo?
cell-mediated immune response which leads to complete loss of melanocytes in affected skin
37
What are langerhans cells and where can they be found?
Langerhans cells are antigen presenting cells (APC) of the immune system which typically reside in the basal cell layer or stratum spinosum
38
What do langerhan cells do?
They survey the skin and present foreign antigens to circulating lymphocytes with the use of extensive cytoplasmic processes
39
What are Merkel Cells?
Merkel cells are neuroendocrine cells involved in mechanoreception located in the basal layer of the epidermis. They sense localized pressure and have slow adaptation (slow to adjust to a constant pressure)
Note: A mechanoreceptor is a sensory receptor that responds to mechanical pressure or distortion. Normally there are four main types in glabrous skin: Pacinian corpuscles, Meissner's corpuscles, Merkel's discs, and Ruffini endings
40
What is a dz associate with Merkel Cells?
Merkel cell carcinoma, derived from Merkel cells, is an extremely aggressive tumor, with a patient prognosis worse than that of malignant melanoma.
41
What layer is thickened in acral skin (soles and palms)
The stratum corneum and it can be up to 0.6 mm
42
What is the dermis comprised of?
It is comprised of primarily of eosinophilic collagen bundles
43
What is the papillary dermis?
The superficial dermis which extends between the rete ridges of the epidermis. Has Type III collagen: loose connective tissue
44
What is the reticular dermis?
The deeper portion of the dermis. Has type I collagen: dense irregular connective tissue
45
What are the 3 main components of the dermis?
Collagen: primarily type I and type III collagen, comprises 70-80% of the dermis
Elastin: 2% of the dermis. provides elasticity
Proteoglycans and glycosaminoglycans: maintain dermal water
46
What is the basement membrane zone?
The BMZ forms the bridge between the overlying epidermis and the underlying dermis.
47
What is a genetic defect associated with the BMZ and what proteins are involved?
Genetic defects in the structural components of the BMZ cause epidermolysis bullosa (EB), a clinical blistering disorder
Genetic defects in A6 integrin, B4 integrin, plectin, and laminin 5 cause hemidesmosomal or junctional subtypes of epidermolysis bullosa (EB), an inherited blistering disorder.
48
What autoimmune dz is associated with BMZ and what genes are involved?
Autoimmune targeting of BMZ proteins BPAG1 or BPAG2. This causes bullous pemphigoid- an acquired, non-inherited auto-immune blistering disorder.
49
What 3 types of secretory glands are there?
Eccrine glands, sebaceous glands, and apocrine glands
50
Which glands are associated with hair follicles and which gland opens directly to the skin surface
Sebaceous glands and apocrine glands are associated with the hair follicle, while the eccrine, or sweat, glands open directly to the skin surface.
51
What do sebaceous glands do?
Sebaceous glands, or oil glands, secrete sebum into the hair follicle. The entire apparatus is called the “pilosebaceous unit”.
These glands shed complete lipid-laden keratinocytes in a fashion termed holocrine secretion.
52
Where are sebaceous glands located?
Sebaceous glands are located throughout the skin, except the palms and soles.
53
What is the role of the eccrine gland?
The primary role of the eccrine gland is thermoregulation via evaporative cooling. Eccrine glands produce hypotonic secretions, known as “sweat”. These glands are not associated with the hair follicle.
54
Where are eccrine glands found?
Eccrine glands are distributed throughout the entire body, with the highest concentration on the palms and soles.
55
What do apocrine glands secrete?
Their odorless secretion, once transformed by skin flora, produces the characteristic “body odor”, or human scent.
56
Where are apocrine glands located?
In the axillae and perineum- they are associated with the hair follicle.
57
What is an example of a modified apocrine gland?
The ceruminous glands of the ear are modified apocrine glands. Together with sebaceous glands they produce cerumen aka ear wax.
58
What does a sebacous gland look like histologically?
Histology of sebaceous glands reveals foamy-appearing lipid-laden cells with small pyknotic nuclei
59
What does an eccrine gland look like histologically?
darkly-staining cuboidal cells surrounding ducts
60
What does an apocrine gland look like histologically?
Apocrine glands show pinching off of the apical cytoplasm of cells lining the lumen
61
What is the pathogenesis of the cutaneous manifestations of miliaria (sweat rash)
Miliaria is obstruction and inflammation of the eccrine sweat ducts, producing a diffuse eruption of tiny vesicles. Because the eccrine glands are not associated with the hair follicle, the small vesicles which characterize miliaria do not correlate with the location of hair follicles. Miliaria crystallina (the mildest form) is a benign condition that is treated with supportive measures only.
62
Explain the anagen, catagen and telogen growth phases of hair growth and how long each one lasts
Anagen: active growth phase. Lasts about 3 years for scalp hair.
Catagen: transitional period, lasting about 3 days for scalp hair.
Telogen: resting phase during which the hair shaft is shed. Lasts 3 weeks for scalp hair.
The adage for time spent in the anagen, catagen, and telogen phases of growth is “3 years, 3 days, 3 weeks”.
63
What is the bulge in a hair unit?
The bulge is located in the outer root sheath at the insertion point of the arrector pili muscle
64
What is the nail plate and nail bed?
The hard part of the nail, the fingernail, is the nail plate. Underlying and adhered to the nail plate is the nail bed.
65
What is the nail matrix and what does it do?
The nail matrix is the germinative epithelium which gives rise to the nail plate and nail bed.
66
What is the luna and proximal nail fold?
The distal aspect of the matrix is delineated by the lunula. The matrix extends proximally beyond the proximal nail fold.
67
What is the eponychium and hyponychium?
The eponychium is the the cuticle at the proximal nail fold, while the hyponychium is the adherent layer at the distal nail fold.
68
What is onychodystrophy?
Onychodystrophy: nonspecific term indicating any abnormality of the nail.
69
What is onycomycosis?
Onychomycosis: fungal infection of the nail plate
70
What is paronychia?
Paronychia: infection of the tissue surrounding the proximal and lateral nail folds
71
What nail manifestation occurs in psoriasis?
Nail pitting (small multiple pits)
72
Therapies used by dermatologists
```
Sunscreens and photoprotection
Topical corticosteroids
Topical immunomodulators
Phototherapy
Lasers
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73
What cases 90% of all skin cancers? What are independent risk factors for skin cancer?
The sun causes about 90% of all skin cancers. The number of blistering sunburns as well as an individual’s lifetime sun exposure are independent risk factors for skin cancer.
It is a common misconception that sun exposure without burning does not increase an individual’s risk of skin cancer. There is no such thing as a healthy tan.
74
What are the 2 categories of sunscreens and how do they work?
Which one degrades with sun exposure?
1. Physical sunscreens, including zinc oxide and titanium dioxide, scatter and reflect UV rays. They are inert and therefore do not degrade with sun exposure.
2. Chemical sunscreens, such as PABA and Parsol 1789, prevent UV rays from reaching the skin through photochemical reactions. Because of their mechanism of action, these types of sunscreens degrade with sun exposure.
75
What is SPF?
Sunscreen SPF, or Sun Protection Factor, is the ratio of the minimal dose of sunlight needed to cause redness of sunscreen-protected skin divided by the minimal dose of sunlight needed to cause redness of unprotected skin. For example, SPF 15 leads to a 94% reduction in skin UV absorption. In order to maintain their SPF, sunscreens should be reapplied every 2 hours. Waterproof sunscreens should be reapplied every 60 minutes to maintain sun protection.
76
What kind of treatment is more often used to treat inflammatory skin conditions?
Topical steroids are a cornerstone in the treatment of many inflammatory skin conditions.
77
What do steroids do?
Steroids directly inhibit the arachadonic acid inflammatory cascade via direct inhibition of phospholipase A2.
Additionally, steroids cause vasoconstriction as well as direct effects on inflammatory cells.
78
Steroids: What does phospholipase A2 do?
Phospholipase A2 cleaves membrane lipids to form arachadonic acid, and ultimately prostaglandins and leukotrienes.
79
How are topical steroids classified?
Topical steroids are classified according to potency.
80
What are Class I steroids?
Class I steroids are “super potent” and include clobetasol (Temovate) and halobetasol (Ultravate).
81
What are class VII steroids?
Class VII steroids are “low potency” and include over-the-counter 1% hydrocortisone.
82
What is an example of a Class IV (mid-potency) steroid?
Triamcinolone acetonide
83
Designate class of steroids to location of body
Different potency topical steroids are used for different locations on the body. Thin-skinned areas of the body with a high degree of vascularity such as the eyelids and genitalia should be treated with low potency (Class 7) steroids. Areas of the body with thicker skin such as the palms and soles are often treated with super potent (Class 1) steroids.Intermediate thickness areas such as the trunk, arms, and legs are most commonly treated with mid-potency steroids (Class 3,4, or 5).
84
Precaution: What steroid classes should be used in children or elderly?
Select less potent steroids in children and elderly patients with thinner skin
85
What is the FTU and how much corticosteroid does it correspond to?
Finger tip unit. Application of topical corticosteroids follow this measurement
1 FTU = amount of medication extending from the fingertip to the first DIP
1 FTU corresponds to 0.5 gm of corticosteroid and will treat 2 palm sizes in the average adult (1 palm size = 1% body surface area)
86
```
How many FTU's for:
2 palms
1 arm
1 leg
Trunk front and back
Whole body surface area
```
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2 palms= 1 FTU= 0.5 gm
1 arm = 3 FTU = 1.5 gm
1 leg = 6 FTU = 3.0 gm
Trunk, front and back = 14 FTU = 7.0 gm
30-45 gm of topical medication are needed to treat the entire body surface area.
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BID application of the entire body surface for two weeks = 800-1200 gm. This is a lot of corticosteroid, considering that a standard tube size is only 30grams!!
87
What are systemic and cuteneous steroid side-effects?
| 5 examples
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HPA axis suppression
Atrophy of the epidermis and dermis
Skin striae (stretch marks)
Telangiectasia
Aggravation of acne
```
ex. Groin striae secondary to inappropriate chronic use of high potency topical steroids.
88
What do NCIs do? (non-corticosteroid immunomodulators)
NCIs inhibit the calcineurin cascade, as does the systemic medication cyclosporine. These agents may be used as an alternative to topical corticosteroids.
89
What are the advantages and disadvantages of NCIs?
Advantages: No side effects seen with chronic corticosteroid use such as skin atrophy, striae, or telangiectasia.
Disadvantages: While these medications are not steroids and therefore do not cause HPA suppression, topical application to a large body surface area can lead to significant medication blood levels with systemic immunosuppression.
Cost! These agents are extremely expensive. A 30gram tube of Elidel is listed at $62.75 on drugstore.com, while an equivalent size tube of 1% hydrocortisone cream is $3.99.
90
What are 2 exmaples of NCIs?
Elidel (pimecrolimus) and Protopic (tacrolimus)
Pimecrolimus is equivalent to a low potency steroid. Tacrolimus, a topical form of FK-506, is a low to mid-potency equivalent.
91
Give 2 examples of dzs treated with UV light exposure?
Psoriasis and mycosis fungoides.
It has specific effects on the cellular and molecular level.
92
What light waves are used
UVB light is 290-320nm. UVA light is 320-400nm.
| Both UVA and UVB light are used to treat skin disorders.
93
What are 3 types of phototherapy?
- UVB
- Narrow band UVB (311nm only)
- UVA + psoralen = PUVA
94
What is the mechanism of action within the skin of phototherapy (3)?
1) Causes pyrimidine dimers, causing cell cycle arrest and inhibition of rapid keratinocyte production seen in certain skin conditions such as psoriasis
2) Induces cytokine production, including IL-1, IL-6, and PGE2
3) Immunosuppressive: alters antigen-presenting function of Langerhans cells
95
What is psoralen?
Psoralen is a photosensitizing agent, first used by the ancient Egyptians to treat skin diseases hundreds of years ago.
96
How does psoralen work?
When oral or topical psoralen reaches its target in the skin, it intercalates between DNA base pairs. Exposure to UVA rays leads to target-specific cell damage by formation of pyrimidine dimers, causing cell cycle arrest and inhibition of rapid keratinocyte production seen in psoriasis skin lesions.
Additionally, the antigen-presenting properties of Langerhans cells to T-cells are directly inhibited.
Infiltrating lymphocytes are strongly suppressed by PUVA. PUVA is a very potent lymphocyte apoptosis inducer. Therefore, diseases known to involve Langerhans cells and T cells in their pathogenesis are responsive to PUVA therapy. These diseases include psoriasis and mycosis fungoides.
97
(Lasers) What is selective photothermolysis?
Selective photothermolysis: laser light is preferentially absorbed by specific chromophores. Chromophores have a specific absorption spectrum. The principle of selective photothermolysis states that laser light will pass through tissue until it reaches a chromophore with an absorption spectrum corresponding the wavelength of laser light.
98
What is a chromophore?
Chromophores are biological molecules such as hemoglobin or melanin. Chromophores have a specific absorption spectrum.
99
What kinds of skin conditions can dermatologists treat using lasers?
Psoriasis, vascular birthmarks, rosacea, acne, and verruca. Can be used to treat nevus flammeus (port wine stain) on the cheek. Hemoglobin is the target chromophore for vascular lasers such as the PDL.
Tattoos (tattoo pigment is target chromophore) and cafe au lait spots (melanin is target chromophore)
100
Risks associated with laser use:
Risks of inappropriate laser use include ocular damage, permanent skin scarring, and permanent abnormal skin pigmentation. Additionally, patients have recently died from lidocaine toxicity secondary to inappropriate use of topical anesthetics prior to laser therapy.
