Intro to dermatology and epidermis Flashcards
The epidermis:
What are its layers?
The epidermis is the outer (epi in Greek meaning “over” or “upon”) of the two layers that make up the skin (or cutis), the inner layer being the dermis.
It provides a barrier to infection from environmental pathogens and regulates the amount of water released from the body into the atmosphere through transepidermal water loss (TEWL). The outermost part of the epidermis is composed of stratified layers of flattened cells, that overlies a basal layer (stratum basale) composed of columnar cells arranged perpendicularly.
Difference between keratinocyes and melanocytes?
Mammalian keratinocytes compose the bulk of the epithelium, undergo keratinization, and form the dead superficial layer of the skin. These superficial keratinized cells are continuously replaced by cells derived from mitotic cells in the lowest layer of the epidermis (i.e., the basal layer). Melanocytes locate in the basal layer and do not keratinize; however, they can produce melanin pigments. Melanin is accumulated in small granules called melanosomes. The melanosomes are transported to dendrites from which the melanosomes are transferred to keratinocytes.
What are the functions of the skin?
A light barrier is provided by the ____1____.
A physical barries and vitamin D synthesis is provides by the ____2____.
Strenght and elasticity is provided by the ____3_____.
Pheromones and body odor is due to ____4_____.
1- Melanocytes
2- Keratinocytes
3- Fibroblasts
4- Apocrine glands
Describe the Fitzpatrick skin types:
Type I: Skin is ________, Freckles______, Sunburn_______, Tan_______.
Type II: Skin is ________, Freckles______, Sunburn_______, Tan_______.
Type III: Skin is ________, Freckles______, Sunburn_______, Tan_______.
Type IV: Skin is ________, Freckles______, Sunburn_______, Tan_______.
Type V: Skin is ________, Freckles______, Sunburn_______, Tan_______.
Type I- white, a lot, always, never
Type II- fair, some, easily, minimally (with difficulty)
Type III: light brown, few, sometimes (initially), average
Type IV- moderate brown, ZERO, minimally, EASILY
Type V- dark brown, ZERO, rarely, dark tan (very easily)
Melanocytes:
What do they produce?
Eumelanin refers to _______ pigment.
Pheomelanin refers to_______ pigment.
–Pigment cells which produce melanin packaged in granules called melanosomes to protect from UV light
Eumelanin: black to brown pigment
Pheomelanin: yellow to red-brown pigment (less effective UV blocker).
Melanogenesis
Defect in tyrosine gene involved in melanin production results in_________
Albinism
Skin pigmentation
How are melanocytes distributed in dark skin?
How are melanocytes distributed in light skin?
What is vitiligo?
Characterized by _______.
It is an autoimmune disorder against the melanocyte.
- Acquired depigmentation
- Microscopic finding is a complete absence of melanocytes
- Commonly seen in periorificial (near body orifices-mouth) and acral (toward peripehery: fingers, hands) locations.
Vitamin D
Deficiency causes______.
It is essential for _______.
In the kidney the active form of vitamin D is __________.
- The sunshine vitamin
- Produced in response exposing the skin to sunlight.
- Also acquired from foods: fish, fish liver oils, egg yolks, and fortified dairy and grain products.
- Vitamin D is essential in bone mineralization
- Deficiency of Vitamin causes rickets (weakened bones causing skeletal abnormalities).
Vitamin D synthesis:
Our skin naturally contains a precursor to vitamin D (7-dehydrocholesterol). When the sun’s ultraviolet rays touch the skin, they convert the precursor to a molecule called vitamin D3 (cholecalciferol), which then follows a metabolic pathway through the liver and finally to the kidneys, where it’s converted into a molecule called calcitriol. That’s the good stuff—the active form. (Vitamin D obtained from food or supplements must also follow that metabolic pathway to become active.)
Basal Cell Layer (Stratum basalis/stratus germinativum)
- Innermost layer of the epidermis
- Contains small round cells called basal cells
- Location of Stem Cells
- Basal cells continually divide, and new cells constantly push older ones up toward the surface of the skin, where they are eventually shed.
- Maturation occurs continuously and renewal of the epidermis takes 28 days
What are hemidesmosomes?
–Attachment point of basal cells to the basal lamina of the dermal- epidermal junction
Antibodies to proteins (230 or 180) in the hemidesmosomes may cause autoimmune blistering diseases such as ____________.
What kind of blisters are they?
What are bulla?
Bullous pemphigoid
- Primary skin lesions are tense bulla
- Pathogenesis: Autoantibodies to BP180 (type XVII collagen) or BP230
- Pathology: *Subepidermal blisters
***Bulla are circumscribed, elevated lesion containing clear serous or hemorraghic fluid that is > 1 cm in diameter.
Epidermolysis bullosa
What are they?
Characterized by ______ formation and response to _________ trauma.
•Epidermolysis bullosa (EB) is a group of inherited bullous disorders characterized by blister formation in response to mechanical trauma.
Types of Epidermolysis bullosa and the level at which they occur in the hemidesmosome:
EB simplex occurs due to defect in ___1____.
EB junctional is due to defects in____2_____.
EB Dystrophic is due to defects in ________.
1- Keratin 5 or 14
2- collagen XVII or laminin 5
3- collagen VII
Junctional EB
Due to genetic defects in ________.
Clinically presents as ______ that improves with age.
Due genetic defects in laminin 5.
Clinical: generalized onset of blisters, improves with age**
Recessive Dystrophic EB
Genetic defects in __________
Extensive dystrophic scarring can produce________ of the hand and feet.
Patients have an increased risk for __________.
Collagen VII
Extensive dystrophic scarring can produce pseudosyndactyly (mitten-hand deformity) of the hands and feet.
-Flexion contractures
Increased risk of ***squamous cell carcinoma
Other complications include infections.
Epidermolysis bullosa simplex
Genetic defects in _________
When do generalized blister occurs at?
What are the most common sites?
Keratin 5 and 14
Clinical: generalized onset of blisters occurs at or shortly after birth.
Hands, feet, and extremities are the most common sites of involvement
Stratum Spinosum
Just above the ______ layer.
- Appears spiny due to the fact that the cells are held together with spiny projections (desmosome attachments).
- The thickest layer of the epidermis, just above the basal layer
- Keratinocytes produce keratin, a tough protective protein that makes up the majority of the structure of skin, hair and nails.
What are desmosomes?
Pemphigus Vulgaris
Characterized by ______ bulla.
They blister are __________.
Acquired antibodies to desmoglein 1 and desmoglein 3
- Primary skin lesions are *flaccid bulla
- Pathogenesis: Autoantibodies to desmoglein 1 and 3
- Pathology: **Intraepidermal blisters
Keratinocytes
Stratus Granulosum
Characterized by the presnece of ______ granules that contain profilagrin (a filaggrin precursor).
Mutation of filagrin leads to DRY SKIN conditions including _____ and ________.
At this layer, what do cells loose?
**Keratohyalin granules contain Profilaggrin (filaggrin precursor). Filaggrin cross-links keratin tonofilaments and is important in the barrier function of the skin.
**Filaggrin is mutated in dry skin conditions including ichthyosis and atopic dermatitis.
- Cells in this layer start to loose their nuclei
- Lamellar bodies excrete lipids (ceramides).
Icthyosis Vulgaris and Atopic Dermatitis
Due to mutation in ______, which causes significant reduced levels of ____ in the stratum corneum and increase transepidermal water loss.
Due to mutated filaggrins
- Defective skin barrier function due loss-of-function filaggrin mutations
- Patients with filaggrin mutations have significantly reduced levels of the NMF in the stratum corneum and exhibit increased transepidermal water loss.
Other notorious cells of the epidermis:
Langerhans cells
–Participate in cell-mediated immunity as antigen presenting cells
Merkel cells
–Small cells associated with nerve endings in epidermis. Their function has long been uncertain, but they seem to be involved in neural development and tactile sensation. Recent evidence supports a role for Merkel cells in light touch.
Stratum Lucidum
The Back
The dermis of the back is the thickest reticular dermis in all of the body (measuring more than 4 mm), and it is made up of broad bundles of collagen.
Although a few eccrine glands can be seen, no apocrine glands are present. Pilosebaceous units are numerous in the midline.
The palms
The skin in these areas is thick to protect against constant friction and pressure. Both areas show a remarkably thick horny layer (compact type) with an accompanying prominent granular layer. The rete ridges are also prominent. These areas are devoid of pilosebaceous units, but they have a high number of **eccrine glands (sweating). Numerous nerve endings are also a characteristic. This hairless, thick skin is also called Glaborus skin.
Flat lesions are:
Macule and patch
Macule–> Circumscribed change in skin color tha is flush with the sorrounding skin <1 cm in diameter. Example:
- -Solar lentigo*
- -Traumatic purpura*
Patch–> Circumscribed change in skin color tha is flush with the sorrounding skin >1 cm in diameter.
- Cafe aut lait spot*
- -Vitiligo*
Raised and Smooth:
Papule
Plaque
Cyst
Nodule
Papule–> A solid or cystic elevation <1 cm in diameter (Acne, Eruptive Xanthoma).
Plaque–> An elevated lesion that is >1 cm in diameter (Psoriasis)
Cyst
Nodule–> A solid or cystic elevation >1 cm but <2 cm in diameter (Dermato-fibroma)
Raised Scaly
*papule with scale/plaque with scale
Scale–> Dessicated, thin plates of cornified epidermal cells that form flakes on their skin surface.
Fluid Filled
vesicle/bulla/pustule
Vesicle–> Circumscribed, elevated lesion containing clear serous or hemorrhagic fluid that is < 1cm (Contact dermatitis, herpex simples).
Pustule–> A vesicle containing purulent exudate (folliculitis).
Redness
Macule
Patch
Papules
Figure A: Smooth papules associated with tuberous sclerosis. Figure B: Erythematous papules in an arthropod reaction.
Plaques
Figure A: Fixed, urticarial plaques with halos.
Figure B: Confluent deep red erythematous plaques of psoriasis.
Nodules
Figure A: Dome-shaped dermatofibroma.
Figure B: Subcutaneous rheumatoid nodule
Surface change
Scale
Figure A: Multiple scaly papules and plaques in guttate psoriasis.
Figure B: Fine scale in tinea corporis.
Crust
Figure A: Green crust in a patient with non-bullous impetigo.
Figure B: Honey-colored crust associated with tinea faciale.
Figure C: Hemorrhagic crusting in a patient with stevens-johnson syndrome
Vesicle
Figure A: Grouped, umbilicated vesicles in a patient with zoster. Figure B: Tense vesicles in dyshidrotic dermatitis.
Bulla
Pustule
Figure A: Multiple pustules on an erythematous base in a patient with pustular psoriasis.
Figure B: Extensive severe pustules in child with pustular psoriasis
Erythema
Erythroderma
Telangiectasias
Figure A: Severe rosacea with large telangectasias of nose in an adult male.
Figure B: Telangiectasia macularis eruptiva perstans in an adult male
Ecchymoses
Petechiae
Palpable purpura
Atrophy
Erosion
Ulcer
Fissure
Figure A: Deep fissures in a patient with dermatitis.
Figure B: Fine fissures of the lower extremity in xerotic dermatitis.
Eschar
Limited distribution
limited distribution
Figure A: Numerous umbilicated vesicles in a dermatomal distribution in a patient with zoster.
Limited distribution
Extensive distribution
Extensive distribution:
Extensive Distribution:
