10. skin Flashcards
what are appendages? what origin are they derived from? where are their bases located?
nails, hairs and glands
epidermal
their bases are located in the lower dermis and subcutis
what is an integument
skin and appendages
what are the two basic types of skin and what does it depend on?
hirsute skin= hairy, dominant
glabrous skin= hairless
only found at
- the epithelial transition zones of the lips and anus
- parts of the outer genitals
- all acral skin
(palmoplantar areas and body protrusions
i.e. toe tips, finger tips, knuckles, elbows, knees)
how can the two different types of skin act in different ways? whats an example of this
acral erythema (redness, swelling)
a common adverse reaction to certain chemotherapy drugs
others: different
sets of mechanoreceptors
innervation of sweat glands
temperature regulation
types of tumours
skin variation
general pattern is the same but layers can vary depending on the body
eg. thinner dermis in flexor side, thick on back
thickness of subcutis varies upon fat storage
function of epidermis
- barrier (permeability & abrasion)
- VitDproduction
- UV protection
- immune defense
- sensory information
epidermal cell types
keratinocytes (90%) : barrier and vit D production
melanocytes: pigment cells, UV protection
* can cause malignancy- 75% death (5% cases)
merkel cells: mechanoreceptor
langerhans cells: dendritic
skin-homing lymphocytes
malignancy in epidermal cell types
basalioma most common
squamous cell carcinoma
melanoma
cutaneous t cell lymphoma, merkel cell carcinoma and langerhan cell histiocytosis are rare
skin cancer: what is the staging based on?
skin layers involved
keratinocyte epithelium
stratified keratinised squamous
granular layer contains dead cells
keratinocyte maturation
- proliferation: constant cell renewal
- differentiation: exit from cell cycle
- mass production: of epidermis-specific compounds (lipids in lamellar bodies, keratins and structural proteins in keratohyalingranules)
- functional re-organisation: of epidermis specific compounds
- cornification= programmed cell death
- desquamation= shedding of surface cells
what is the concept of the barrier of keratinocytes
brick wall
corneocytes= bricks: strengthened cornifiedenvelope made out of structural proteinsand tonofibrils
Corneodesmosomes= Rivets hold the cellular sheet together
Extruded lipids = Mortar
arranged in multi-lamellar membrane sheets prevent trans-epidermal water loss
how does the stratum corneum (outermost layer of the skin) act as a permeability barrier?
highly lipophillic structure
the intercellular space is filled with multi-lamellar sheets of extruded lipids
sealed with natural moisturizing factor (NMF)
- collective term for filaggrin-derived compounds
- bind about 20% of water
properties of stratum corneum
water repellent
can be crossed by low Mr lipophillic substances
prevents trans epidermal loss of water and solutes
what must the cornified layer be in order to repel water?
hydrated!
- NMFs absorb water and swell, sealing the intercellular space
- this allows the cornified layer to stay hydrated
- as NMFs are water soluble, they easily leach from the cells upon water contact
- i.e. too immersion in water actually makes the skin drier
what substances can be absorbed trans dermally
- most organochlorineinsecticides
- solvents
- fumigants
(skin absorption common route for pesticide poisoning)
skin patches (eg. nicotine)
keratinocyte adhesion
what is desquamation
is strictly controlled process where proteases are degrading the corneodesmosomes
The integrity of the epidermis depends on the cohesion between keratinocytes, with desmosomesas the main adhesion structures
issues arising relating to adhesion
not strong enough:
defective adhesion leads to fluid accumulation between cells and the formation of blisters
too strong:
hereditary altered structure of keratins or structural proteins delay the rate of desquamation
UV damage to skin
UVA indirect DNA damage via formation of free radicals
photodegradationof certain vitamins (e.g. folate) in dermal capillaries?
UVB direct DNA damage (disrupted DNA replication)
and sunburn
endocrine function of skin
- Vitamin D is naturally present in very few foods
- It is also produced endogenously in the epidermis upon UVB radiation
- lack of epidermal production has to be fully compensated by dietary intake (or vice versa)
UVBrays are required for photoconversion of 7-DHC into VitD3 by keratinocytes in the Malpighian layer
protection against UV rays
- UV-induced DNA damage in keratinocytes leads to p53-mediated up-regulation of proopiomelanocortin (POMC)
- posttranslational cleavage of POMC produce α-MSH and ACTH which bind to the melanocortin1-receptor (MC1R) on melanocytes and induce melaninproduction
- melanin-containing organelles = melanosomesare passed on to keratinocytes
- melanin absorbs UV light and transforms the energy into heat
happens when skin is already damaged
what is natural skin colour determined by
- the rate of melanin production (melanogenesis)
- the chemical structure of melanin
- the degree of melanizationof melanosomes
- melanosomenumbers, dispersion and turnover
- pigmentsother than melanin (haemoglobin, carotene)
