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Block 1 Week 3 > Skin > Flashcards

Skin Flashcards

1
Q

What is skin (x8)?

A

1) protective barrier against chemical, physical and infectious insults
2) accounts for 16% of the body’s weight
3) thickness & structure varies
4) mobile & elastic
5) involved in thermoregulation (via sweat & vasculature)
6) important in blood pressure reg (uses capillary beds)
7) sense organ (touch/pain)
8) tells you stuff as physician about state of the patient

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2
Q

Skin layers?

A

1) epidermis = epithelium = keratinized stratified squamous
2) dermis = connective tissue under epithelium
3) hypodermis = looser connective tissue under that

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3
Q

How nourish the epidermis?

A
  • same as all epithelia
  • nourished by diffusion from capillaries under the basement membrane
  • the capillaries are in the dermis layer
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4
Q

where is the basement membrane at in a skin tissue slide?

A
  • basement membrane is at the dermal/epidermal junction
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5
Q

what does Retin A do?

A

-stimulates neovascularization in the dermis which increases rate of basal cell proliferation

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6
Q

How do you increase basal cell proliferation?

A

-by increase the amount of nutrients being absorbed by the basal cells

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7
Q

Where are the capillaries that nourish the epithelial layer?

A

-the capillaries are in the dermis layer

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8
Q

what do you know about the relative activity of the cells closest versus farthest from the source of nutrients?

A

the closer cells (on the basement membrane; nearest the dermis which houses the capillaries) are most actively dividing since receive the most nutrients

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9
Q

thick vs thin skin?

A
  • refers only to the dermis

- can have thin epidermis and thick dermis, but is still thin skin

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10
Q

Thick skin found?

A
  • areas of high wear and tear (palms, soles of feet)
  • is usually highly keratinized
  • is crucial to keep dermial-epidermis layers together but is harder to do w/ thick skin
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11
Q

how keep dermial-epidermis layers together?

A
  • need extensive epidermal-dermal junctions (layers)

- done by forming lots of epidermal pegs/dermal papillae (3D ridges)

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12
Q

Thin skin?

A
  • is typical of most other parts of body besides those that get a lot of wear & tear
  • skin very thin to retain flexibility & elasticity
  • membrane is wavy
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13
Q

Why is thin skin basement membrane wavy?

A
  • increased access to capillaries
  • increases stretchy/elasticity of tissue
  • increase tissue mobility, required for skin
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14
Q

Papillae/ridges pattern?

A
  • seen in the keratin layer (epidermis layer)

- produces finger prints

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15
Q

How get separation between cells in the epidermis (epithelial cells)?

A

-repetitive movements causes a separation between cells in the epidermis

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16
Q

What happens when get separation between cells in the epidermis?

A
  • blister (fluid-filled pocket) will form

- if viruses/ bacteria can get in can form pustules

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17
Q

How get blood blister?

A
  • if have separation between the epidermis & dermis

- small capillaries will break giving you blood blister

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18
Q

Purpose of the dermis? Composition?

A
  • located just under the epidermis
  • is composed of loose connective tissue (lots of elastin, collagen T1 &T3) smooth muscle cells
  • gives mobility to the surface layers of the skin
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19
Q

Which components of connective tissue are being referred to as loose or dense?

A

-collagen, elastic fibers, smooth muscle, fat all work together to determine dense vs loose connective tissue

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20
Q

What happens to elastic fibers as we age?

A

We begin to loose elastin/fibril so our elastic fibers loose their ping back, our skin gets saggy

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21
Q

What fibers stop you from over-stretching the skin? What happens if you rip these?

A
  • the elasticity of elastin fibers
  • if rip the elastic fibers, skin looses ability to ‘ping back’ is get saggy skin
  • collagen also puts thresholds on skin stretching, if loose collagen T1/T2 now can overstretch the skin
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22
Q

Dermis Pathology?

A

-a connective tissue disease
-due to defects in dermis collagen deposition
-dermis usually loose;
ex 1: excessive fibrosis (fibroid) cause abnormal (intense) wound healing
ex 2: scleroderma

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23
Q

excessive fibrosis (fibroid) due to?

A

connective tissue dermis layer have fibroblast that lay down collagen; if over active get fibrosis

  • cause scars/scar tissue,
  • an exaggerated wound healing response, cause organ damage
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24
Q

scleroderma due to?

A
  • inflammatory infiltrates drive excessive collagen deposition leading to loss of skin elasticity
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25
Q

What are the layers of the epidermis in the skin?

A

1) Keratin layer: cornified (tough protective layers) of cells are dead
2) stratum spinosum
3) basal lamina layer of epithelial cels

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26
Q

Keratin layer of the skin

A
  • outer most skin layer; epithelial cells
  • cornified (tough protective layers) of cells are dead
  • can be 1 or 2 cells thick or very thick
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27
Q

stratum spinosum layer?

A
  • granular and prickle cell layer
  • provide separation between dividing cells and dead cornified cells at the top
  • often times have lost nuclei in this layer
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28
Q

cornified mean?

A

tough protective layer of the skin

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29
Q

basal lamina layer of epithelial cels?

A
  • divide to give rise to the cells above, but they only do so at night
  • create water tight seal by constantly dividing and making differentiating cell types
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30
Q

How basal lamina create water tight seal?

A
  • by establishing intercellular conenctions

- by forming dehydrated, keratin layer of cells that are dead and

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31
Q

clear cells? what are the 4 types?

A
  • in basal and prickle cell layers
  • all dendritic, w/ cytoplasmic extensions in & among other cells
  • involved in immune responses
    1) melanocyte
    2) Merkel cell
    3) Langerhans cell
    4) gamma delta T lymphocyte
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32
Q

How are clear cells distinguishable?

A

-have central nuclei with (colored) with a clear cytoplasm around it, different than epithelial cells

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33
Q

Melanocytes

A
  • a clear cell
  • responsible for skin&hair color
  • melanin-producing neural crest-derived cells
  • under dermis layer of skin
  • embryologically late migrating cells from the neural crest
  • retain their mobile characteristics & plasticity throughout life.
34
Q

Melanocytes mechanism?

A
  • in -early development, neural crest-derived melanocyte progenitor cells line up down spine, migrate through body from there
  • lots of genes effect melanin
35
Q

Melanocytes and neurotransmitters?

A
  • have similar movements to neurons
  • way pigment granuels are move & deopisited in skin/hair follicles, similar to how neurotransmitter pushed arund in neurons
  • often see pigment & neurotranmitter diseases because of it
36
Q

Melanin

A
  • made from tyrosine in granules which budded off the Golgi
  • Mature melanin granules exocytosed from melanocytes (in dermis) their content is endocytosed by basal cells and prickle cell
37
Q

What is a melanoma vs. basal cell carcinoma severity?

A

melanoma is worse because has mobile characteristics throughout life
-so can move through body; basal cells do not

38
Q

Melanocytes and wound healing?

A

-wounds initially white, take time to develop color because takes time for melanocyte cells to migrate from neural crest to reach the injury

39
Q

Variations in skin color occur because of?

A
  • All races have same # of melanocytes variation depends on:
    1) rate of synthesis of melanin
    2) size of melanin granule
    3) ability of other cells to endocytose melanin granule core
    4) types of melanin produced
40
Q

Two types of melanin?

A

pheomelanin versus eumelanin

41
Q

pheomelanin versus eumelanin

A

1) blondes produce more light pheomelanin

2) darker skinned peoples produce more eumelanin

42
Q

advantage/disadvantage of fair skin?

A
  • can absorb more UV to make Vitamin D

- is easily damaged by too much UV

43
Q

advantage/disadvantage of dark skin?

A
  • protection from UV

- reduced ability to make Vitamin D

44
Q

Merkel cell?

A
  • clear cell
  • modified nerve endings
  • contain neurotransmitter granules (amount varies w/ skin region)
  • mechanoreceptors in hair follicles (tell you if your face is being touched)
45
Q

Langerhans cells

A
  • clear cell
  • born in bone marrow; constitute 4% of epithelial cells
  • are self-renewing in skin, have slow turnover/replacement from bone marrow
  • are skin dendritic cells
46
Q

Langerhans cells & immune response? Unstimulated vs stimulated state?

A
  • are the skin’s Dendritic Cells
  • express immune Antigen Presenting Cell markers such as MHC Class II antigens
  • typicallly reside in an nstimulated resident state,
47
Q

Langerhans cells cytoplasm?

A

-tennis racket-shaped Birbeck “granules”which can appear appear in regular macrophages in some disease states

48
Q

Langerhans cells in unstimulated state?

A

-in unstimulated resident state, they are not as potent as lymphoid tissue Dendritic Cells

49
Q

Langerhans cells in activation?

A

activation by inflammation or cytokines

  • causes upregulation in stimulatory molecules
  • induces their migration into draining lymph nodes to trigger immune responses
50
Q

What do tissue dendritic cells (Langerhans) stimulate?

A

-trigger organ graft rejection

51
Q

Gamma-delta T Cells?

A
  • found in all epithelia, but in diff variations depending on the tissue
  • produce growth factors important for wound healing/ tissue repair from inflammation & infections
52
Q

What clear cells have similar morphologies

A

malanocytes, gamma delta T cells and langerhans have similar morphologies

53
Q

Prickle Cell layer ?

A
  • also called stratum spinosum
  • cells remain stuck together by desmosomes, can’t shrink
  • main structural cells of the epidermis
  • when dehydrated; form tight connections, in H20 would swell if they were only cells in the epidermis
54
Q

why called prickle cell layer?

A
  • cells appear to have prickles at under light microscope

- is an artifact of tissue dehydration & shrinkage

55
Q

Keratinization

A
  • keratins produced in all normal epidermal cells;
  • increasing #; type & distribution; and amount of cross linking change w/ distance from the basement membrane
  • form waterproof barrier
  • form cornfield layer and are dead at this pint
56
Q

thicker keratin layer?

A

the greater the protection

57
Q

creating of the cornfield layer?

A
  • as cells move through layers of prickle cells, they produce molecules that act as a glue between cells
  • sticks cells to one another over entire surface, forms waterproof barrier
  • lysosomal digestion of organelles make cells dead bags of keratin
  • thicker keratin=more protection
58
Q

keratin & expression of tight junctions?

A

-Is limited and transient.

59
Q

Warts

A

example of Keratinocyte patholology

-HPV drive keratinocyte proliferation leading to thickening at the dermoepidermal junction

60
Q

Epidermal Involutions (papila) of the skin?

A
  • provide sites for skin repair if the surface epithelium is lost
  • body can do it on own, also seen in treatment of burns
  • allows for split skin grafting.
61
Q

split skin grafting process?

A

do basememnt membrane transplant to give burn victims an active epithelial cell layer
-the epithelial cells will grow out of glands & hair follicles, provide new skin tissue

62
Q

Hair

A
  • a type of holocrine secretion
  • cells remain stuck together
  • cell division in basal layer gives rise to cells above that gain more & more keratin.
63
Q

hair color?

A

Melanocytes contribute color to the hair in the same way as in the rest of the skin
-grey hair due to melanocytes not migrating anymore

64
Q

estrogen/ testosterone and hair growth?

A
  • head hair, estrogen stimulates growth
  • in presence of some pituitary factors, testosterone inhibits growth
    • castration cure balding
    • estrogen treatment increases hair growth
65
Q

Abnormal hair growth in women

A

-most often due to adrenal production of androgens

66
Q

Goosebumps

A
  • Cold initiates contraction of smooth muscle
  • squishes skin in angle to make a goose bump
  • squeezes sebum out of the sebaceous gland & makes hair stand up straight
67
Q

Sebaceous Glands

A
  • empty into hair follicles
  • testosterone promotes cell division; estrogen inhibits
  • secret oily material
  • are sacs of lipids
  • natures moisturizers
68
Q

Sebaceous Glands secretions?

A
  • as cells move farther from basement membrane, they accumulate lipid & die
  • dead bags of lipid move onto the skin surface
  • easy for exit of glands to get blocked
69
Q

Sebaceous Glands blockage?

A
  • blockage w/ increased cell division, may result in cells bursting through basement membrane
  • initiates an inflammatory response in the dermis(acne)
  • clogging& inflammatory responses are exacerbated by bacteria in hair follicle
70
Q

Follicle Mites

A
  • can block sebaceous glands

- many black heads are follicle mites (demodex folliculorum). )

71
Q

Sweat Glands

A

-simple coiled tubular glands
-secretions=H20, ions & nitrogenous waste
-Stratified cuboidal
-

72
Q

Sweat Glands secretions provess?

A
  • secretory portion produces initial product
  • duct modifies product ( by reuptake of sodium)
  • specific chloride channels are required for reuptake, are dysfunctional/absent in CF
  • is why CF patients have very salty skin, cells can’t uptake Na from skin
73
Q

Sweat Glands & thermoregulation?

A
  • Sweat comes up through ducts & empties onto the surface
  • Evaporation cools skin surface, which cools blood in capillary beds in the dermal papillae
74
Q

Apocrine Sweat Glands

A
  • secrete in both apocrine & merocrine fashion
  • large secretory regions
  • empty into hair follicles, which serve as the ducts
  • found in axillary regions (not useful for thermoregulation) & produce pheromones
75
Q

Apocrine Sweat Glands

secretions?

A
  • water, ions, protein and lipid
  • bacteria cause apocrine secretions to smell bad
  • release pheromones
  • secretions accelerated by contraction of myoepithelial cells
76
Q

Fingernails

A
  • nail similar to hair but w/ harder keratin
  • white part (lunulae) due to active dividing epithelium, younger & healthier people have larger ones
  • Cells divide in basal layer & move at angle to surface during keratinization
77
Q

nail clubbing?

A
  • excessive nail curvature due to circulatory disorders and insufficient oxygenation of blood in extremities
  • may show as blue nail beds
78
Q

Nerve Endings In Skin?

A
  • pain and fine motion detectors
  • have different functions
  • often require special stains
    1) Meissner’s Corpuscle
    2) Pacinian Corpuscles
79
Q

1) Krause end bulbs?

2) Ruffini corpuscles?

A

1) cold receptors

2) sit on collagen fibers, stretch receptors

80
Q

Meissner’s Corpuscle

A
  • responsible for sensitivity to light touch
  • Schwann cells are parallel to skin surface
  • Lateral movement of skin distorts the cell and is transmitted to a nerve fiber
  • common in dermal papillae/ridges
81
Q

Pacinian Corpuscles

A
  • large deep pressure receptors
  • push on your skin; these tell you where pushing
  • mostly in hypodermis
  • tell you when your bladder is full
82
Q

Pacinian Corpuscles mechanism?

A

Schwann cells are arranged at 90 degrees to skin surface so pressure will compress them
- this communicated to the afferent fiber

Block 1 Week 3 (8 decks)

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