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Medicine 1 > 10. skin > Flashcards

10. skin Flashcards

1
Q
A
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2
Q

what are appendages? what origin are they derived from? where are their bases located?

A

nails, hairs and glands

epidermal

their bases are located in the lower dermis and subcutis

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3
Q

what is an integument

A

skin and appendages

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4
Q

what are the two basic types of skin and what does it depend on?

A

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)

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5
Q

how can the two different types of skin act in different ways? whats an example of this

A

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

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6
Q

skin variation

A

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

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7
Q

function of epidermis

A
  • barrier (permeability & abrasion)
  • VitDproduction
  • UV protection
  • immune defense
  • sensory information
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8
Q

epidermal cell types

A

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

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9
Q

malignancy in epidermal cell types

A

basalioma most common

squamous cell carcinoma

melanoma

cutaneous t cell lymphoma, merkel cell carcinoma and langerhan cell histiocytosis are rare

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10
Q

skin cancer: what is the staging based on?

A

skin layers involved

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11
Q

keratinocyte epithelium

A

stratified keratinised squamous

granular layer contains dead cells

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12
Q

keratinocyte maturation

A
  1. proliferation: constant cell renewal
  2. differentiation: exit from cell cycle
  3. mass production: of epidermis-specific compounds (lipids in lamellar bodies, keratins and structural proteins in keratohyalingranules)
  4. functional re-organisation: of epidermis specific compounds
  5. cornification= programmed cell death
  6. desquamation= shedding of surface cells
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13
Q

what is the concept of the barrier of keratinocytes

A

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

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14
Q

how does the stratum corneum (outermost layer of the skin) act as a permeability barrier?

A

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
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15
Q

properties of stratum corneum

A

water repellent

can be crossed by low Mr lipophillic substances

prevents trans epidermal loss of water and solutes

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16
Q

what must the cornified layer be in order to repel water?

A

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
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17
Q

what substances can be absorbed trans dermally

A
  • most organochlorineinsecticides
  • solvents
  • fumigants

(skin absorption common route for pesticide poisoning)

skin patches (eg. nicotine)

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18
Q

keratinocyte adhesion

A
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19
Q

what is desquamation

A

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

20
Q

issues arising relating to adhesion

A

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

21
Q

UV damage to skin

A

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

22
Q

endocrine function of skin

A
  • 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

23
Q

protection against UV rays

A
  • 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

24
Q

what is natural skin colour determined by

A
  • 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)
25
Q

what type of trait is skin colour?

A

polygenic

determined by the additive effects of an estimated 125 different genes

  • perhaps 7 gene products have the most impact, with MC1Rbeing the most important
  • MC1R regulates both the quality and quantity of melanin production
26
Q

the two different waves of melanocyte migration from neural crest

A

ventral wave- schwann cell precursor cells in dermis-> epidermal melanocytes

dorsal wave: melanocyte stem cells->hair bulb melanocytes

27
Q

why can hair and skin have different colours?

why can children from biracial parents show different skin colour?

A

different melanocyte populations

alleles of skin colour randomly distribute

28
Q

2 main types of melanin

A

eumelanin: pale, medium, dark tan and blonde- black hair
pheomelanin: no tan, red hair (no protection)

29
Q

pigmentation problems

A
30
Q

function of dermis

A

supplies the epidermis

  • fluid storage
  • thermoregulation
  • wound healing
  • strengthand elasticity
  • immune defence
  • sensory structures
  • appendages
31
Q

function of hypodermis/ subcutis

A
  • fat storage
  • insulation
  • padding
  • sensory structures
  • appendages
32
Q

how is the cutaneous blood supply organised?

A

3 horizontal plexus

The skin has a low metabolic rate, i.e. most blood flowing to the skin has a thermoregulatory rather than a metabolic function

blood supply of the skin is directly linked to the blood supply of the underlying skeletal muscles

33
Q

what is the epidermis in terms of blood supply?

A

avascular

supplied by diffusion of dermis

  • Dermal papillae greatly increase the contact area between dermis and epidermis
  • they contain a plexus of capillaries and lymphatics
  • can contain encapsulated mechanoreceptors (Meissner’s corpuscles)
  • cause ridges in the overlaying epidermis = fingerprints
34
Q

discuss the papillary layer in the dermis

A

loose connective tissue

supplies epidermis

stores fluid

immune defence

papillary layer

  • thin fibre bundles; arranged randomly
  • highly capillarisedand hydrated
35
Q

discuss reticular layer of dermis

A

dense connective tissue

strength and elasticity

  • thick fibre bundles; arranged orthogonally
  • abundant elastic and collagen fibres

(70% collagen and 1% elastin)

36
Q

what do mechanoreceptors do?

A

sense mechanical pressure or distortion of surrounding

37
Q

types of mechanoreceptors in glabrous skin

A
38
Q

“pilo-sebaceous unit” or “follicular unit”

A

The actual hair follicle

+ arrectorpili muscle

+ sebaceous gland

39
Q
A

acne- result of blocked infibidulum

40
Q

sebaceous glands

what is sebum

A
  • mixture of mostly nonpolar lipids
  • coat the fur as a hydrophobic protection against overwetting and for heat insulation
  • Increased sebum excretion is a major factor involved in the pathophysiology of acne
41
Q

where are apocrine glands found and what are they

what is apocrine sweat

A

sweat glands

certain regions (eg. axilla)

become active during puberty

cloudy, viscous fluid- proteins, lipids, steroids

presence of bacteria causes odour

evolved to coat and stick to hair

42
Q

eccrine sweat glands

A

dominant type of sweat gland (secretes directly to surface)

only gland not associated with hair

own separate excretory duct: acrosyringium

clear hypotonic fluid

43
Q

evolution of sweat glands

A

primates show a transition from apocrine to eccrine gland-dominant skin

  • original eccrine glands remain in the palmoplantar and cranial regions
  • original apocrine glands remain in the axilla and perineal region
  • new eccrine glands take over the limbs and trunk
44
Q

thermoregulation

A

Our evolutionary old and new glands are differently regulated

cholinergic (PNS): newly evolved eccrine glands (trunk and limbs)

a-adrenergic (SNS): conserved glands

eccrine= palmoplantar & cranial

apocrine = axilla, perineum

(explains sweating patterns when under stress)

45
Q

why can glabrous skin get colder than hirsute

A

glabrous skin has extra atriovenous shunts so more blood reaches surface

open during hypothermia

Medicine 1 (53 decks)

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