derm 2 Flashcards

1
Q

Function of the hair (6)

A
Protection against external factors
Sebum- oily substance on our skin 
Apocrine sweat
Thermoregulation
Social and sexual interaction
reservior for Epithelial and melanocyte stem cells
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2
Q

what is Terminal hairs

A

scalp, eyebrows and eyelashes, beard

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3
Q

what sort of hair covers the rest of our body

A

vellus hairs

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4
Q

what regions have no hair

A

(except palms, soles, mucosal regions of lips, and external genitalia.

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5
Q

what are the stages to hair cycle (3)

A

Anagen
Catagen
Telogen
(then loss of hair)

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6
Q

what is anagen

A

where new hair forms and grows

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7
Q

catagen

A
regressing phase(hair is shrinking)
lasts 3 weeks
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8
Q

telogen

A
resting phase (blood supply removed from hair)
lasts 3 months
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9
Q

what is a hair follicle

A

pilosebaceous follicles

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10
Q

where does the sebaceous gland open

A

at the hair follicle

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11
Q

what sort of muscle is the Arrector pili

A

smooth muscle

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12
Q

what orientation is it

A

extends at angle between surface of dermis and point in follicle wall.

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13
Q

Holocrine sebaceous glands which open into the ….

A

pilary canal → in axillae - follicles associated with apocrine glands.

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14
Q

what is the Infundibulum

A

Uppermost portion of the hair follicle extending from opening of sebaceous gland to surface of the skin

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15
Q

what is the sebaceous gland (function)

A

secreates sebum

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16
Q

what is the isthmus

A

Lower portion of upper part of hair follicle between opening of sebaceous gland and insertion of arrector pili muscle

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17
Q

where is the buldge

A

Segment of the outer root sheath located at insertion of arrector pili muscle

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18
Q

what is special about the buldge

A

hair foliicle stem cells reside there

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19
Q

what happens if they migrate downwards

A

generate the new lower anagen hair follicle → enter hair bulb matrix, proliferate and undergo terminal differentiation to form hair shaft and inner root sheath.

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20
Q

and upwards

A

form sebaceous glands and to proliferate in response to wounding

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21
Q

function and location Outer root sheath (ORS)

A

Extends along from the hair bulb to the infundibulum and epidermis serves as a reservoir of stem cells

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22
Q

function of Inner root sheath

A

Guides / shapes hair

Encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fiber & capillary loop.

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23
Q

Function of the nails (5)

A

Protection of underlying distal phalanx
Counterpressure effect to pulp important for walking and tactile sensation
Increase dexterity / manipulation of small objects
Enhance sensory discrimination
Facilitate scratching or grooming

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24
Q

how is the nail plate made

A

Final product of proliferation and differentiation of nail matrix keratinocytes- lose organelles and become keratin

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25
Q

what is the only visible part of the nail matrix

A

lunula

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26
Q

how does the nail matrix produce the nail plate

A

Nail matrix keratinocytes differentiate → lose their nuclei and are strictly adherent - cytoplasm completely filled by hard keratins

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27
Q

does it contain melanocytes in the matrix

A

yes

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28
Q

what does white or red show on skin

A

red- inflammation

white- keratin

29
Q

what is Psoriasis

A

Chronic, immune-mediated disorder

30
Q

can a genetic predispostion cause it

A

not enough on its own, need enviromental triggers

31
Q

what are the cells involved

A

involves T-cells and their interactions with dendritic cells and cells involvement in innate immunity, including keratinocytes

32
Q

what does it cause on the skin

A

(chronic plaque psoriasis) Sharply demarcated, scaly, erythematous plaques characterise the most common form of psoriasis

33
Q

where is it commonly found

A

of involvement are scalp, elbows and knees, followed by nails, hands, feet and trunk (including intergluteal fold)

34
Q

doe sit just invlove the skin

A

Psoriatic arthritis is most common systemic manifestation

35
Q

what is the pathophysiology in psoriasis

A

Stressed keratinocytes release DNA / RNA → form complex with antimicrobial peptides → induce cytokines (TNF-α, IL-1 and IFN-α) production → activate dermal dendritic cells (dDCs)

36
Q

what do the dermal dentrictic cells do

A

dDCs migrate to lymph nodes → promote Th1, Th17, Th22 cells → chemokine release – migration of inflammatory cells into dermis → cytokine release → keratinocyte proliferation → psoriatic plaque

37
Q

what are the clinical features

A

plaques/scales,

can occur on the nails

38
Q

what is erythroderma

A

inflammation that occurs to more than 90% of skin, lose the skin properties like more vunreable to infection

39
Q

what can aggrivate psioris

A

smoking and drinking

40
Q

how is it managed

A

Topical therapies
like vit d analogs or vit a analogs

phototherapy- causes t cell apoptosis
narrowing UVB
PUVA

41
Q

what is atopic eczema

A

Intensely pruritic chronic inflammatory condition

42
Q

what is pruritic

A

causes itching

43
Q

is it enviro or gentic

A

both

44
Q

when does it start

A

infancy or early childhood

45
Q

what is the difference between eczema and dermatitis

A

nothing

46
Q

how to treat

A

Daily emollients and anti-inflammatory therapy are cornerstone of management

47
Q

what is the function of Filaggrin

A

bind and aggregate keratin bundles and intermediate filaments to form cellular scaffold in corneocytes

48
Q

what is the diff in the filaggrin with people with eczema

A

muatated filaggrin

49
Q

function of corneocytes

A

essential part of skin barrier. property

50
Q

what is a resuolt of this

A

increase transepidermal water loss (TEWL)

51
Q

what does that cause

A

Impaired protection against microbes and environmental allergens

52
Q

what causes the inflammation

A

Staphylococcal superantigens stimulate Th2 lymphocyte responses and subvert T‐reg
SPCL find the skin of eczma more hospitable

53
Q

are eosinophils inlvoled

A

yes

54
Q

what signs/symo of eczema are there in skin

A

Acute inflammation of cheeks, scalp and extensors in infants

55
Q

and adults/children

A

Flexural inflammation and lichenification in children and adults

thikening of skin due to extensive/chronic ithcing

disorded pigmentation
exgerrated of normal skin marking

56
Q

what happens when you lose the hydration of the epidermis

A

less flexible
casuing fissuring
v painful affect quality of life

57
Q

what is Allergic contact dermatitis

A

allergic caused by contact with substance

58
Q

what is a feature of Atopic eczema
(Impetiginisation)
what pathogen causes it

A

Gold crust

Staphylococcus aureus

59
Q

what is Venous stasis eczema

A

is a long-term skin condition that affects the lower legs

barrier function lost

60
Q

what are erosions

A

breaches to epidermis that dont go all the way thru- if they did they would be ulcers

61
Q

what is Eczema

herpeticum

A

emergency, not to be confused with eczema
breakdown of the skin barrie
more pron to herpes virus

62
Q

how to treat atopic eczema

A
Lifestyle
Emollients (at least 3 times a day)
Omission of soap
Clinical Nurse Specialist involvement
Topical application technique
Day treatment
Habit reversal(stop them itching)
Co-morbidities
63
Q

how to tell that it is not due to allergy

A

Patch testing

Biopsy

64
Q

when would you do biopsy

A

nipple eczema that dioesnt repsond to treatment

to exclude pagents disease

65
Q

Adverse effects of topical corticosteroids:

A

Rare: skin atrophy, folliculitis, exacerbation of acne and rosacea, infection
Very rare: perioral dermatitis (right), rebound syndrome (tachyphylaxis), allergy (to steroid itself or vehicle)
Extremely rare: hormonal imbalance (suppression of hypothalamic-pituitary-adrenal axis), hirsuitism
Adverse effects of topical calcineurin inhibitors:
Burning sensation

66
Q

what is the aporcrine gland

A

a modified suncaoues gland

67
Q

how many layers do soles and palms have

A

5 (lucidium is only in the soles and palms)

68
Q

the evapouration of sweat which cools you down

epinochyiom

A

in the exam