Basic Science of Skin

atopic dermatitis

barrier dysfunction of filaggrin

impetiginized mycosis fungoides

skin lymphoma due to lymphocyte dysfunction

lymphocyte sydfucntion fo skin can lead to

cancer, allergy, infection, inflammation

erythrodermic

more than 90% of skin is red or inflamed

cutaneous vasodilation when extensive can cause hypothermia and cardiac failure

HIV associated lipotrophy

loss of fat throughout face

layers of the skin

epidermis: mainly keratinocytes

dermis: fibroblasts, collagen I and elastic fibers. flexible, thick and supportive. binds water. has blood vessels, lymphatics and nerves. hair follicles, swear and glands

subcutis: fat that insulates and cushions, also allows for mobility

hair follicle vs. sebaceous gland location

hair follicle: spans the subcutis and reticular dermis

gland: just in the reticular dermis superficially

morphea

loss of subcutis causes skin to be bound down

erythema nodosum

inflammation of the subcutis

deep nodules on the shine

can be from underlying enteric or lung inflammation

layers of the epidermis

Superficial to deep:

Stratum Corneum

Stratum Granulosum

Stratum Spinosum

Stratum Basale

MNEUMONIC: Camille's Grandma Sends Billions.

order skin cells mature

from bottom up over 2 week life cycle

cells differentiate as they move up toward top

basal layer

source of epidermal stem cells

cell division occurs here

keratinocytes start here and move upwards

spinous layer

center of epidermis

desmosomal junctions hold the keratinocytes together giving spiny appearance

granular layer

lipids are made by the keratinocytes here

forms a water barrier in the ECF to keep water in the skin

stratum corneum

desquamating keratinocytes

thick layer of flattened cells, non-nucleated

barrier against trauma

filaggrin

protein in granular cell layer for barrier funciton

mutation in this causes atopic dermatitis and asthma

bullous pemphigoid

loss of adhesion of skin layers - autoimmune blistering beneath basal epidermis (roof) and dermis (floor)

tense bullae

usually in elderly

pemphigus vulgaris

loss of adhesion of skin layers - autoimmune blistering disease where antibodies attatch keratinocytes to each other

flaccid bullae, erosions and mucus membrane impacted

usually in young to middle aged adult

psoriasis

rate of epidermal turnover is increased

over proliferation of keratinocyte causes plaque and cells cannot differentiate and slough off

scales in the corneal (outermost) layer

basal cell carcinoma

these cancer cells will resemble basal keratinocytes

appears pearly, erythematous papule or plaque with rolled border and telangiectasis

in sun exposed areas

cell types of the epidermis

keritonocytes: main

-held together by desmosomes "spines"

melanocytes: 2nd most popular

-staggered on basal layer

-produce pigment

langerhans cells:

-dendritic cell

-immune function: can exit dermis to travel to lymphomas

merkel cells:

-mechanoreceptor cells for touch in basal layer

contact dermatitis

can be from poison oak

langerhans cells where they uptake antigen and exit epidermis to travel to lymph node and ignite immune response

Merkel cell carcinoma

aggressive rare skin cancer

deep pink to red nodules

mimic furuncle or cyst

pilosebaceous unit

1 hair follicle & it's associated:

1. sebaceous (oil) gland, 2. apocrine (sweat) gland

3. arrector pili muscle

layers of the dermis

superficial to deep

papillary dermis

reticular dermis

Ehlers-danlos syndrome

collagen type I or III genetic disorder

hyper-extensible joints

skin or vascular aneurysms

loose weenis

solar elastosis

chronic UV exposure causes degradation of collagen and elastic fibers

cell types of the dermis

fibroblasts:

- synthesis and degradation of connective tissue proteins

-key in wound healing/scarring

mast cells:

-lead to immediate hypersensitive runs in the skin

urticaria

vascular reaction in skin with wheals surrounded by red halo

keloids

abnormal scarring due to uncontrolled synthesis and deposition of collagen at sites of prior dermal injury

keratosis pilaris

disorder of keratin retention

fordyce spots

prominent sebaceous glands of genital skin and mucosal surfaces

acne vulgaris

1. plugged follicle due to keratinization

2. c. acnes bacteria in follicle

3. hormones (androgens)

4.sebacous gland activity increased by androgens

eccrine sweat glands

do not involve hair follicle

open directly onto skin surface

regulate body temp etc

if absent a patient can get hyperthermia

hyperhydrosis

overstimulation of eccocerine glands by acetylcholine by sympathetics

adnexal structures in dermis

hair follicles

apocrine and eccrine sweat glands and sebaceous glands