VPHY 3108 test 2 skin

Hypodermis function and structure and layer:

bottom layer Subcutaneous tissue/fat- insulation and energy

Dermis layer number and what it contains?

middle layer, hair, blood vessels

Fibroblasts, macrophages, mast cells

layer of dermis

- Particular layer (bottom, 4/5 of dermis)

- Papillary Layer (top, 1/5 of dermis)

Particular layer

Itch/stretch and pressure receptors, Dense irregular tissue (structure and support)

Papillary layer

epithelial maintenance

capillary loops

free nerve endings (pain/tactile)

areolar connective tissue

capillary loops

exchange nutrient and waste

fluid balance

heat transfer

immune

Dermal papillae and epidermal ridge functions

border btw dermis and epidermis

locks layer

skin furrows and fingerprints

blisters

grip

Epidermis function

Protection- keratinized stratified squamous epithelium, 4 or 5 layers- keratinocytes

Epidermis layers bottom to top

Stratum basale → stratum spinosum → stratum granulosum → stratum lucidum → stratum corneum

Stratum Basale cells

Basal (stem cells)

Tactile cells (merkel)

Malanocytes

basal cells

mitotic cells- cell division

spawn keratinocytes

demosomes

Stratum spinosum

desmosomes connection btw keratinocytes--> spiny

Production of lamellar bodies and keratinocytes- not released yet

dendritic cells

stratum granulosum

Keratohyalin granules

hard protein envelope

lamellar bodies release lipids

cells die

stratum corneum

30 layer of compact dead keratinocytes

lipid rich intercellular matrix

Keratinocytes life

stratum basale: mitosis

stratum spinosum: keratin fiber, lamellar bodies

stratum granulosum: lipids release, keratin, surrounded by lipids

what causes perspiration

sudiferous/sweat glands

vasodilation:

vasoconstriction:

vasodilation: dissipate heat

vasoconstriction: retains heat

cold vs hot peripheral hair

cold: sweat secretion stop, piloerection- hair stands up

hot: sweat glands secret, pilorelaxation- hair flattens

Physical vs chemical barrier

physical: junction, layers, keratin

chemical: epidermal lipids, natural moisturizing factors, low Ph

Low PH:

skin: filaggrin degradation

moisture: lipid degradation

-- maintain ph

acidic PH: controls enzymes for lipids synthesis, microbiome and diversity

sebum vs sweat

sebum: protects an dlubricates hair and skin

sweat: water, salt, fatty acids, metabolic waste, ph:4-6

Glands distribution eccrine vs apocrine

Eccrine: all over

Apocrine: sweaty areas

acid mantle:

exocrine secretion- ph of skin slightly acidic

Barrier to UV light

melanin- protein, protect keratinocytes from dna damage

UVA, UVB, UVC

A: aging, blocked by sunscreen, not glass, longest wavelength, damage collagen and elastin, indirect dna damage

B: burn, blocked by sunscreen and glass, skin burns, direct dna damage

C: short wavelenth, does not reach earth

melanin

protects dns--> absorbs harmful rays

uemelanin= stronger

pheomelanin= weaking

skin tone is ratio of these

Melanocytes

produce melanosomes

activity varies- increased by uv exposure

melanosomes

membrane bound organellar storing and exporting melanin

phagocytosed by keratinocytes

Skin cancer types and severity

Basal cell- least severe

squamous cell

melanoma- most sever

types of skin cancer

Basal- stem/basal cells, permanently disfiguring

squamous- keratinocytes, metastasize if not removed

melanoma- melanocytes, highly metastatic, chemotherapy resistant

Dendritic (Langerhans) cells steps

1) phagocyte eats bacteria

2) antigen goes to surface of phagocyte

3) presents antigen to helper t cells

4) helper t cell activated

Cytotoxic, helper, regulatory t cells

Cytotoxic: produce toxic agents to kill

helper: stimulate B cells to make antibodies, stimulate T cells to activate

regulatory: suppress immune response

phagocytes types and function:

Neutrophil: intracellular degradation elimination of invading microorganisms

Dendritic cell: induction of adaptive immunity by presenting antigens to T cells

Macrophage: elimination of exogenous pathogens as well as host derived molecules including dead cells

Wound healing stages

hemostasis, inflammatory, proliferative, remodeling

stages of wound healing functions and time:

Hemostasis: Hours, blood clot, coagulation

Inflammatory: days, early reparative response, sterilization of dead cells, lymphocytes, scabs, phagocyte recruitment

proliferative: 1-2 weeks, re-epithelialization, granulation, wound contractive, fibroblast activation, lymphocyte recruitment

remodeling: 1-2 weeks, collagen deposition, ecm, scars, healed

Hemostasis purpose and activities

Blood loss prevention, vasoconstriction, platelet aggregation, fibrin clot

Primary hemostasis:

vascular spasm-constriction, platelet activation, aggregation via fibrinogen plug, vasoconstriction

secondary hemostasis

coagulation cascade

2 pathways:

- intrinsic: within vessel

- extrinsic: outside of vessel

goal is to stabilize clot

prothrombin--> thrombin

Mast cells histamine and heparin

Histamine: vasodilation- increased blood flow and vessel permeability

Heparin: anticoagulant

3rd degree burn

no dermis remains, risk of fluid loss, infection, no pain, down to subcutaneous tissue

The liver during coagulation

Fibrogen and prothrombin made in liver, bile salts make vitamin K

Inflammation purpose and function

- clean wound and reduce risk of infection

- increased blood flow and capillary permeability for immune cells to move

- mast and macrophages recruit immune cells (mast: histamine= redness and swelling) (macrophages release cytokines)

- Neutrophils arrive first, other later

Proliferation purpose and processes

- restore the structural integrity of the tissue

- angiogensis

- granulation

- epithelialization

Angiogensis:

formation of new capillaries to supply nutrients and oxygen to repairing cells- rebuild tissue

granulation:

fibroblasts produce collagen- structure

collagen pulls wound together

epithelialization

macrophages remove clot, restoration of skin barrier by epithelial cells multiplying and migrating

Remodeling purpose and processes

collagen replaced by stronger collagen, capillary removal (avascular tissue)

Regeneration vs Fibrosis

Regeneration: replacing damaged tissue , restores function and shape

Fibrosis: scarring, replacing damaged tissue with collagen, not normal function

why would a wound be slow to heal?

damage--> apoptosis--> oxidative (kills cells) stress --> impairment