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Disease and Defense III > Dermis and Adnexal > Flashcards

Dermis and Adnexal Flashcards

1
Q

What is contained within the dermis? (3)

A

blood vessels
nerves
appendageal strutures (hair / glands / etc)

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2
Q

what provides the major tensile strength of the skin?

A

the dermis

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3
Q

Thickness of the dermis

A

varies by local (1-4 mm)

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4
Q

Where does the dermis lie?

A

between the epidermis and sub-cu

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5
Q

what are the appendageal structures ?

A

hair
sweat gland
sebaceous gland
vessels and nerves

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6
Q

what are the two major zones of the dermis?

A

papillary

reticular

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7
Q

papillary dermis -
location?
content?
interlocks with?

A

upper layer of dermis
thin collagen bundles
interlocks with epidermal rete

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8
Q

the interlocking of the dermis with the epidermal rete increases (2)

A

strength and surface area

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9
Q

reticular dermis
location?
content?

A

deeper layer

thick collagen bundles
visible eslatic fibers

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10
Q

what are the three building blocks of the dermis?

A

collagen
elastic fibers
ground substance

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11
Q

structure of collagen in the skin ?

A

alpha helical
Gly-X-Y
X = proline
Y = hydroxyproline

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12
Q

How many types of collagen are synthesized in the body

A

> 25

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13
Q

G-X-Y of collagen

what are X and Y

A

X proline

Y hydroxyproline

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14
Q

Which collagen is in greatest abundance in the skin?

A

collagen I

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15
Q

what percent of the adult dermis (wt) is collagen I

A

85%

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16
Q

which collagen is largest part of fetal dermis

A

III

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17
Q

Which collagen makes up the BM

A

IV

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18
Q

Which collagen is responsible for anchoring fibrils

A

VII

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19
Q

_________________ are characteristic of mature collagen?

A

“pretty” 68nm bands

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20
Q

Where is PROcollagen synthesized?

A

within firboblasts

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21
Q

What happens to PROcollagen?

A

excreted extracellularly

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22
Q

What happens once PROcollagen is excreted extracellularly

A

it is enzymatically cleaved to TROPOcollagen

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23
Q

What happens once TROPOcollagen is produced in ECM?

A

It aggregates and becomes crosslinked

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24
Q

Cross-linking of Tropo-collagen is dependent on?

A

Vitamin C

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25
Q

What results from VitC deficiency

A

Scurvy

decreased mature collagen

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26
Q

What would we call VitC

A

Cofactor

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27
Q

How long does it take to manifest sign/symptom of VITC deprivation?

A

1-3 months

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28
Q

Key findings of scurvy?

A

keratotic plugging of hairs
perifollicular hemorrhage
“corkscrew hairs”
hemorrhagic gingivitis

weakened / delayed healing

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29
Q

Why does hemorrhage occur in scurvy?

A

Lack of collagen support for blood vessels leads to rupture and hemorrhage (same for gums)

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30
Q

What kind of disease of collagen production would we call scurvy?

A

acquired

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31
Q

What is a congenital problem of collagen disease?

A

Ehlers Danlos Syndrome

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32
Q

Ehlers-Danlos Syndrome

family of disorders based upon?

A

erroneous collagen synthesis

mutation at various stages of collagen production

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33
Q

Ehlers-Danlos Syndrome - mutations at various stages of collagen production yield findings such as… (4)

A

hyperextensible skin
hyperextensible joints
fragile blood vessels
poor wound healing

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34
Q

What might you be tempted to think Ehlers Danlos is a disorder of?

A

Elastic fibers! But resist the temptation! It is a disorder of collagen production

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35
Q

Gordin’s sign

A

characteristic of EDS - touch tip of tongue to nose

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36
Q

Molluscoid pseudotumors

A

characteristic of EDS

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37
Q

Absence of the inferior labial frenulum can often be seen in

A

EDS

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38
Q 
Elastic fibers - constitution of dermis?
function
size?
distribution?
visualized?
A

minor constituent of dermis

provide resliency

thin fibers (1-3 micro-meter)

intertwined among collagen bundles

special stains are required to visualize (VVG)

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39
Q

Our example of acquired disorder of elastic fiber

A

Solar elastosis

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40
Q

Solar elastosis

A

acquired disorder of elastic fiber

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41
Q

solar elastosis visualizing ?

A

basophilic (blue) material within superficial dermis

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42
Q

If we see basophilic material within superficial dermis - this is a histologic clue that we are observing?

A

Tissue from an older person in sun-exposed skin - Solar elastosis (sun damaged elastic fibers) - we would not expect to see this in children

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43
Q

What is an example (We discussed) of an acquired disorder of elastic tissue?

A

pseudoxanthoma elasticum

-

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44
Q

pseudoxanthoma elasticum is caused by a mutation in?

A

MDR gene

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45
Q

pseudoxanthoma elasticum results in

A

calcified, brittle elastic fibers

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46
Q

which disease is associated wtih

- plucked chicken skin

A

pseudoxanthoma elasticum

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47
Q

pseudoxanthoma elasticum is associated wtih
skin finding?
system finding?
eye finding?

A

plucked chicken skin

systemic hypertension - with arterial rupture (particularly eye)

angioid streaks in the retina

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48
Q

Ground substance - made up of?

A

protein-sugar moieties (glycosaminoglycans) - hyaluronic acid and dermatan sulphate

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49
Q

what glues together the protein-sugar moeities of the ground substance?

A

fibronectin

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50
Q

what is an acquired disorder of ground substance? stretch

A

cosmetic hyaluronic acid filler may (Sometimes) represent an acquired disorder of ground substance

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51
Q

what congenital problems do we see with ground substance?

A

none

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52
Q

Blood vessels in the epidermis

A

none

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53
Q

where does epidermis get its nutrient / oxygen supply?

A

depends entirely on the dermis via diffusion

54
Q

Two plexi of skin vessels?

A 
superficial plexus (goes in dermal papillary loop)
deep plexus (with perforating arterioles)
55
Q

disorders of capillary loops?

A

dilated, torturous capillaries are noted with diseases with increased epidermal turnover - psoriasis / verruca

56
Q

when do we see dilated capillaries (which recall are in dermis) with epidermal diseases?

A

diseases with increased epidermal turnover - e.g. psoriasis / verruca (warts)

57
Q

what causes vasculitis

A

inflammation of capillaries and venules due to immune complexes depositing in small vessel walls

58
Q

immune complexes in vasculitis may result from?

A

drug hypersensitivity
infection
neoplasm
collagen vascular disease

59
Q

what type of immune reaction is vasculitis of the dermal capillaries?

A

type III - antibody mediated so will positive coomb

60
Q

What notable finding will we often see with vasculitis?

A

palpable purpura

61
Q

what is palpable purpura -

A

combination of inflammation and hemorrhage that manifests frequently with vasculitis of the dermal capillaries - extravasation can also contribute to palpableness :)

62
Q

Nervous tissue of the dermis?

job?

A

inform and protect

63
Q

nerves traverse the dermis to end as?

A

specialized nerve structures (Meissner / Pacinian)

free nerve endings

64
Q

Two important types of nerve fibers to be aware of?

A

A and C

65
Q

Type A nerve fibers

characteristic

A

heavily myelinated and conduct rapidly

66
Q

Type C nerve fibers characteristic

A

unmyelinated and conducts slowly

67
Q

Four types of A fibers?

A

A -alpha –
A - beta
A - gamma
A - delta

68
Q

A-alpha fibers

A

proprioception and large motor units (largest)

69
Q

A-beta fibers

A

carries touch

70
Q

A-gamma fibers

A

spindle organs in teh muscle stretch receptors

71
Q

A-delta fibers

A

smallest - fast localizing initial component of pain

72
Q

Type C fibers job

A

convey sensation of diffuse, dull, non-localizing / temp and itch sensations

73
Q

what is itch called?

A

pruritis

74
Q

4 common causes of itch

A

Dry skin (xerosis)
Infection (HIV)
Infestation (scabies / lice)
metabolic disorders (renal failure)

75
Q

Meissner’s corpuscles

A

pine-cone like structures located near the DEJ inovlved in fine touch, highest density on the pulps of digits

76
Q

Pacinian Corpuscles

A

onion like - structures located in the dermis, involved in pressure and vibration - highest in the genitals

77
Q

Adnexal structures (5)

A 
hair follicles 
eccrine glands
apocrine glands
apoeccrine glandes
sebaceous glands
78
Q

Basics of hair

Types of hair (2)

A

terminal

vellus

79
Q

terminal hair

A

dark / thick / course

80
Q

vellus hair

A

fine / thin / apigmented

81
Q

Hair follicle anatomy is divided into 3 regions

A

infundibulum / isthmus / matrical region

from bottom to top

82
Q

Which fibers are responsible for itch?

A

Type C fibers

83
Q

Embryologic origin of hair?

A

Primitive ectodermal germ (PEG)

Classic induction

84
Q

Embryologic origin of hair - induction?

A

mesenchyme induces the overlying neuroectoderm –> downward bud with 3 bulges

85
Q

hair gland 3 bulges?

A

upper - apocrine (+/-)
middle - sebaceous gland
lower - attachment arector pillori

86
Q

How many hairs does the normal scalp contain

A

> 100,000

87
Q

3 cycles of hair

A

anagen (growth) 85%
telogen (rest) 10-15%
catagen (involution) 1-5%

88
Q

3 cycles of hair and the rule of three?

A

anagen - 3 years
telogen - 3 months
catagen - 3 weeks or less

89
Q

androgenic (androgenetic) hair loss?

A

“pattern baldness”
characteristic loss
50% population
conversion of testosterone to DHT results in miniaturization of follicle

90
Q

treatments of hair loss

A

finasteride (propecia) - selective inhibitor of 5-alpha reductase
- blocks conversion of testosterone to DHT
- works well in prevent loss and “less well” in restoring hair loss IN MEN
Dangerous in women of reproductive age! ?post-menopause

91
Q

Fiansteride and hair loss

Women?

A

NO! do not use in women of reproductive age!

- blocks conversion to T to DHT and seems to help men from losing more

92
Q

What happens to the hair follicle followin finasteride treatement?

A

follicles go deeper in dermis

93
Q

Sebaceous glands - purpose?

A

lubricate thick terminal hairs

94
Q

acne pathogenesis

disease of?

A

disease of pilosebaceous unit

95
Q

acne is a disease of pilosebaceous unit - there is abnormal?

A

follicular maturation

96
Q

abnormal follicular maturation in acne causes ?

A

comedone formation (black-heads / white-heads)

97
Q

acne - following the comedone formation that resulted from abnormal follicular maturation what happens?

A

the plugged follicular environment allows overgrowth of P acnes

98
Q

What does P acnes do in acne?

A

P acnes liberates FFAs and or rupture follicles –> later events yield dermal inflammation

99
Q

Holocrine glands -

A

whole cells are shed and disintegrate, release contents

100
Q

which are quintessential holocrine glands?

A

sebaceous glands

101
Q

Eccrine glands -

A

odorless watery sweat glands

102
Q

Eccrine glands are important in -

A

thermoregulation

103
Q

where are eccrine glands numerous?

A

forehead - cutaneous lip - palms/soles

104
Q

eccrine glands produce what type of secretions

A

merocrine

105
Q

what are merocrine secretions?

A

excreted via exocytosis from secretory cells into an epithelial-walled duct or ducts and thence onto a bodily surface or into the lumen

106
Q

innervation of eccrine glands?

A

sympathetic - but use ACh

107
Q

Are eccrine glands derived from primitive ectodermal germ?

A

No!

108
Q

Which glands are derived from PEG (primitive ectodermal germ?)

A

Upper = apocrine
Middle - sebaceous
Lower - errector pili attachment

109
Q

Eccrine gland anatomy?

A

sweat production - beginning is located way down between the junction of the dermis and sub-cu — then travels up long long tube all the way through the dermis and through the epidermis - until it is release onto the skin.

110
Q

2 acquired disorders of sweating?

A 
heat shock (classic)
antiperspirants
111
Q

Heat shock -

A

you stop sweating and overheat

112
Q

How do antiperspirants work?

A

active agent - AlClOH3, selectively soluble

perspiration raise the pH - insoluble precipitates to block sweat duct

washing with soap raises pH - solublel –> duct is unblocked

113
Q

What is miliaria?

A

prickly heat :) / or sweat gland gets ruptured - sweat goes into dermis where it is not supposed to be and causes prickly heat
blocked sweat ducts

114
Q

miliaria in bambinos –>

A

febrile

115
Q

what is an acquired disorder of eccrine function?

A

miliaria

116
Q

are there congenital problems of eccrine function?

A

anhidrotic ectodermal dysplaisa

117
Q

what is anhidrotic ectodermal dysplaisa?

A 
mutation in EDA gene 
Aberrant eccrine development 
severely decreased sweating
poor temp regulation 
other ectodermal problemos - sparse hair / abnormal teeth
118
Q

If we see someone come in with decreased sweating / temp regulatory problemos / and other ectodermal problems e.g. hair/teeth… what might we consider?

A

anhidrotic ectodermal dysplasia

119
Q

apocrine glands are?

A

outgrowths of the upper bulge of primitive ectodermal germ

120
Q

where are apocrine glands located?

A

axillary and anogenital area

121
Q

when are apocrine glands functional

A

usually post puberty

122
Q

specialized apocrine glands (3)

A

Moll’s (eyelid)
cerumen (external auditory canal)
lactation (boobs)

123
Q

how do apocrine glands secrete?

A

decapitation

124
Q

how is apocrine sweat different than eccrine

A

stickier (sialomucin)

125
Q

odor of apocrine sweat?

A

initially odorless but flora of normal skin make smelly

126
Q

apoeccrine glands =

A

hybrid sweat glands

located mainly in axilla

127
Q

apoecrrine glands - likely play role in?

A

axillary hyperhidrosis

128
Q

apoeccrine glands secrete how much sweat relative to eccrine?

A

nearly 10x

129
Q

Treatment of hyperhidrosis?

A

botulinum toxin

130
Q

How does botox treat hyperhidrosis?

A

block acetylcholine release - upon which secretion is dependent!

Disease and Defense III (11 decks)

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