derm A Flashcards
learn
skin- other pathologies
psoriasis, dermatitis, infections, toxin exposure
- ~psoriasis: ~8-9 million in US population (chronic inflammatory skin disease –> impact on QOL and skin function)
skin structure and function: barrier has cellular basis?
epidermal:
- cell-cell and cell-matrix connections, extracellular lipids.
skin structure and function: Epidermal renewal and repair?
- stem cell replication
- hyper-proliferative pathologies
skin structure and function: skin adexnal structures?
- hair and sebaceous glands
- nails
- sweat glands
skin the reductionist approach: epidermis
- keratinocytes, melanocytes, langerhaan cells. (barrier structure & function from keratinocytes)
- barrier function is mostly held within the first 2 cell layers in the epidermis (essential)
- flat cells in the epidermis help barrier function (shape change to flat further towards the surface)
- keeps germs and toxic shit out.
skin the reductionist approach: dermis
extracellular matrix proteins & diverse cell types (blood vessels, glands, nerve endings, base of hair follicles)
- papillae hold layering together
- hypodermis below dermis
Skin- tissue overview
- skin (also known as integument) is the largest organ, variable thickness
- Composed of two tissue layers: surface (cellular epidermis –> one cell on top of another), lower (mostly acellular dermis –> small amount of fibroblasts but surrounding is made of mostly noncellular material such as collagen, a connective tissue)
skin- epidermal functions
- Protection from physical-chemical trauma, desiccation
- ~1/10th of entire skin thickness
- metabolic – synthesis of vitamin D
- Antigen up-take (langerhans’ cells –> immune system derived) –> there are not a lot of langerhans cells by %, but there are a lot in total because of the large surface area of the epidermis
- No blood vessels –> nutrients come from blood vessels in the dermis
Skin- Dermal functions
- Sensation: support for nerve endings
- Blood vessels: nutrient supply for epidermis and dermis thermoregulation via dilation and constriction.
- blood vessels are larger in the RETICULAR LAYER and are finer capillaries in the PAPILLARY LAYER (more densely packed collagen)
https://o.quizlet.com/KPXA.d-BMVpm3GYX9i4-8w.png
melanocytes: epidermal
-melanocytes, MCs (pigment cells) –> skin and hair pigment
- ~5% of epidermal cells
- “clear” cytoplasm –> light in color themselves
- ~1 melanocyte for 10-20 basal keratinocytes
- make melanin (pigment) and ships the pigment off to surrounding cells called keratinocytes
- arborized/dendritic
epidermis- Melanin
- production stimulated by endocrine & paracrine signals at melanocortin receptor
- delivered to & phagocytized by KCs
- KCs are packed with intermediate filament protein = keratin
- partly digested by KC lysosomes
- accumulates over KC nucleus
- scatters & absorbs UV light
- forms a protective cap over the genetic material of keratinocytes to decrease mutations and carcinogenesis of UV light
epidermis - melanin variation in density across body surface
- regional concentration (nevus or “mole”) –> leads to a small group fo keratinocytes with a lot of melanin but still normal/healthy
- ABCDE’s of moles: asymmetry, border, color, diameter, elevation
- change may indicate malignancy (dysregulation of melanocytes)
- ex. smaller than the width of a pencil eraser is usually fine, flatter elevation is less worrying
epidermal pigmentation
melanin: 2 types –> skin and hair are a balance of the two
- brown-black, eumelanin
- reddish-yellow, phaeomelanin
- ratio determines pigmentation; eumelanin more photoprotective
- both increase in response to UV light –> melanin production is stimulated by UV light (ex. tanning)
- triggered by MSH (melanocyte-stimulating hormone = melanocortin)
- binding membrane melanocortin receptor
- overall pigmentation –> combination of MSH levels (signal), MSH-receptor activity, melanin production
- freckles = keratinocytes concentrated melanin from melanocytes
epidermal pigmentation - vitiligo
localized, progressive loss of pigmentation
- incidence: ~1/100; all races & both sexes are affected
- autoimmune destruction of MCs; associated with other autoimmune diseases, ex. pernicious anemia
- proteins are seen as foreign antigens –> destruction of self-proteins
- deficit of color = MC destroyed
epidermis cell types: langerhans’ cells (LC)
- <5% of cells in epidermal layer
- bone marrow-derived –> migrate from circulation across basement membrane into epidermis
- function as part of immune system –> surveillance
- phagocytize & process low MW antigens (poison ivy/oak) into LCs
- exposure to antigen triggers migration of LC to regional lymph nodes
- LC breakdown antigens & present them to other immune cells in lymph nodes (hand off which completes immune response)
- large surface area of skin provides increased opportunity for antigen detection & initial processing (increases absolute number)
- ex. allergic reactions)
epidermis cell types: keratinocytes
- ~90-95% of all cells in epidermis
- upper epidermal layers called stratum corneum show body site specification in response to pressure or friction –> mostly due to changes in thickness of cornified layer (accumulation of cells in the layer)
- possible “clear layer” –> stratum lucidum (tightly packed squames seen in high frictional stress areas; palms & soles)
- all sites eventually & normally desquamate –> loss of squames (continual turnover to maintain integrity)
epidermis - keratinocyte layers
- basal layer = stratum germinativum
- spinous layer = stratum spinosum
- granular layer = stratum granulosum
- cornified layer = stratum corneum
LOOK AT PICTURE
epidermis - keratinocyte basal layer (stratum germinativum)
- mitotic in normal epidermis
- migrate into wound to cover site
- the only place with cell replication
- made of mostly basal cells –> above this layer are postmitotic
epidermis - keratinocyte spinous layer (stratum spinosum)
- cells are post-mitotic but still very metabolically active (keratin protein production, etc.)
- numerous cell-cell attachments = desmosomes –> responsible for “spine-y” histology & much of epidermal structural strength
- physical connections keep epidermis layer intact
epidermis - keratinocyte granular layer (stratum granulosum)
- keratin proteins aggregate (granules)
- nuclei breakdown; lipids extruded
- other specialized proteins are chemically x-linked resulting in increased mechanical resistance
- when cells leave the granular layer they die
epidermis - keratinocyte cornified layer (stratum corneum)
- cells cease metabolism
- cells flatten into discs = squames; eventually lost
- 3–4 weeks from basal to cornified layer
epidermis - structure & differentiation
bricks & mortar” (derived from keratinocytes)
- two biochemical phases in granular & cornified layers
- proteins in cells cross-linked together –> hydrophilic “brick” (make up 1 keratinocyte packed with keratin protein)
- lipids in extra-cellular space –-> hydrophobic “mortar” (extrude through cell)
- both are a challenge to transdermal drug delivery but also part of the barrier function of epidermis
epidermis: chemical barrier
- slows transit of water-soluble AND lipid-soluble compounds
- advantages / disadvantages: lessens dehydration of underlying tissue & entry of toxins BUT restricts cutaneous drug delivery
epidermis: physical barrier
desmosomes between cells provide structural integrity / strength
