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BRS - Dermatology > Intro to Derm Part 2 > Flashcards

Intro to Derm Part 2 Flashcards

(58 cards)

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1
Q

what are the functions of the hair

A

Protection against external factors

Produce sebum (produce by pilosebaceous unit)

Apocrine sweat (odour sweat in armpit and gential region)

Thermoregulation

Social and sexual interaction

reservoir of epithelial and melanocyte stem cells

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2
Q

what are the different types of hair

where are they

A

terminal hair (thick) - on scalp, eyebrows, eyelashes

vellus (thin and pale) - on rest of body except palms, soles, mucosal regions of lips, and mucosal regions of external genitalia.

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3
Q

what is the hair cycle

how long does hair stay in each phase

how much of our hair is in each phase

A

Anagen - where new hair forms and grows

➢85% of hair is in this phase; lasts 2-6 years

Catagen (regressing phase) hair is shrinking

➢1% of hair is in this phase; lasts 3 weeks

Telogen (resting phase) - durin this phase blood supply is removed from hair

➢10-15% of hair; lasts 3 months

shortly after Telogen phase finishes the old hair is lost

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4
Q

what is a pilosebaceous unit

what makes up pilosebaceous unit

A

hair shaft, hair follicle, arrector pili muscles, sebaceous gland

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5
Q

what are hair follicles

A

epidermal invagination which projects into the dermis

envelops small papilla of dermis at the base

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6
Q

what is the structural difference between eccrine and apocirne sweat glands

A

eccrine sweat gland opens directly onto most superficial layer of epidermis (skin surface)

apocrine sweat gland is a modified sebaceous gland - so opens into pilary canal of hair follicle

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7
Q

what is the arrector pili

where is it

what does it do

A

smooth muscle which extends at angle between surface of dermis and a point in follicle wall

part of pilosebaceous unit

raises hair - important in thermoregulation

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8
Q

label this diagram

A
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9
Q

how is the hair follicle divided

A

infundibulum - uppermost portion of the hair follicle extending from opening of sebaceous gland to surface of the skin

isthmus - lower portion of upper part of hair follicle between opening of sebaceous gland and insertion of arrector pili muscle

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10
Q

what type of secretion do sebaceous glands carry out

A

holocrine

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11
Q

what is the bulge

what is its function

A

segment of the outer root sheath - located at the insertion of the arrector pili muscle

hair follicle stem cells reside here

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12
Q

how do hair follicle stem cells work

A

migrate from the bulge either downwards or upwards (distally)

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

upward (distally) - to form sebaceous glands and to proliferate in response to wounding – replace keratinocytes

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13
Q

what is the bulb of the hair follicle

A

lowermost portion of the hair follicle

includes follicular dermal papilla and hair matrix

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14
Q

what is the outer root sheath of the hair follicle

where is it

A

reservoir of stem cells

extends along from the hair bulb to the infundibulum

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15
Q

what is the function of the inner sheath of the heair follicle

what is its structure

A

guides the hair growth outwards and shapes the hair

encloses folliclular dermal papilla - which contains nerve fibre (provides sensation), capillary loop, mucopolysaccharide rich stroma (structural support)

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16
Q

what are the functions of the nails

A

Protection of underlying distal phalanx

Counterpressure effect to pulp of skin - important for walking and tactile sensation

Increase dexterity / manipulation of small objects

Enhance sensory discrimination

Facilitate scratching - get rid of parasities etc or grooming

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17
Q

label the structure of the nail

A
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18
Q

how is the nail plate produced

what is its structure

what is its growth rate

A

final product of proliferation and differentiation of nail matrix keratinocytes - have lost all their organelles and nuclei, just dense keratin now

emerges from proximal nail fold and detaches at hyponychium

firmly attached to nail bed

lined laterally by nail folds

grows 1-3mm/month

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19
Q

what is the nail matrix

where is it

what happens there

A

site of nail plate synthesis

Lies under proximal nail fold, above bone of distal phalanx (to which it is connected by a tendon

lunula is the only visible portion of the nail matrix

nail matrix keratinocytes differentiate ⇒ lose their nuclei ⇒ become strictly adherent - their cytoplasms become filled with hard keratin

contains melanocytes but they are inactive

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20
Q

what is the lunula

A

only visible portion of the nail matrix

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21
Q

what is shown in these pictures

what has caused this

A

redness - due to inflammation

white scale - keratin

scaly red erythamatous plaques

caused by psoriasis

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22
Q

what is psoriasis

how do people get it

A

chronic immune-mediated disorder

it has a polygenic disposition combined with environmental triggers e.g. trauma, infections, or medications

(genetic predisposition will not cause disease manifestation, need environmental triggers as well)

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23
Q

what are the characterisitics of psoriasis

A

Sharply demarcated, scaly, erythematous plaques

commonly located on scalp, elbows and knees, followed by nails, hands, feet and trunk (including intergluteal fold)

systemic inflammation - liver

Psoriatic arthritis is most common systemic manifestation (but can get this without having psoriasis)

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24
Q

describe the pathophysiology of psoriasis

Study These Flashcards
A

keratinocytes are put under stress, (this can be caused by trauma, drugs, microbes)

stressed keratinocytes release DNA / RNA

DNA/RNA forms complex with antimicrobial peptides (which are produced by keratinocytes - defensins, cathelicidines, psoriasin)

complex formation induces cytokines (TNF-α, IL-1 and IFN-α) production

cytokines produce cascade which results in activation of dermal dendritic cells (dDCs)

once activated dDCs migrate to lymph nodes and promote production of Th1, Th17, Th22 cells

the T cells then produce chemokines which cause migration of inflammatory cells (e.g. neutrophils) into dermis

inflammatory cells release more cytokines in the dermis which activates keratinocytes to proliferate (defence mechanism)

keratinocyte proliferation causes psoriatic plaque to form

25
what are these what causes them
erythamatous scaly plaques scale is keratin occurs in psoriasis progressive differentiation of keratinocytes happens at a much faster rate than usual and in a disorderly fashion so keratinocytes are unable to differentiate properly
26
how can psoriasis on the breast and groin be different to the usual presentation why
flexural psorisasis not as much scale present due to friction
27
what is shown in this picture what does it suggest
nail psoriasis - where psoriasis affects the nail matrix large effect on quality of life, difficult to treat signifies much higher risk of psoriatic arthritis subungal hyperkeratosis - scale forming underneath distal end of nail plate onycholysis - separation of distal nail from nail bed oil stains - due to nail lifting of nail bed pitting of nail plate - stressed keratinocytes which make up nail plate are inflamed so are not adhering to each other effectively
28
what condition is show here what can cuase it to develop
guttate psoriasis tear drops plaques classically follows streptococcal throat infection
29
how is psoriasis treated (without medication)
secondary prevention: minimisation or avoidance of aggravating factors - alchol and smoking (as well as active treatment)
30
what are the co-morbidities associated with psoriasis
higher risk of: coronary heart disease inflammatory bowel disease - some psoriasis treatments can treat this condition but some aggravate it e.g. anti TNF mental health conditions e.g. depression, anxiety - especially due to aesthetic appearance
31
give an overview of the active treatment of psoriasis
therapeutic ladder: 1st line = topical therapies - Vitamin D analogues, Topical corticosteroids, Retinoids – vitamin A analogues and phototherapy, Topical tacrolimus / pimecrolimus 2nd line = systemic treatment - Acitretin, methotrexate, ciclosporin 3rd line = systemic treatment - PDE4 inhibtors, biologics, JAK inhibitors
32
what is the first line treatment for psoriasis
33
what are the possible side effects of phototherapy to treat psoriasis
causes apoptosis of T cells in skin - so affects skin immunity may cause herpes outbreak if already infected (doesn't affect systemic immmunity) PUVA carries skin cancer risk but UVB doesn't
34
what are the second line treatments for psoriasis
35
what are the 3rd line psoriasis treatments
36
describe the symptoms shown what does this child have
Scaly, crusty oedematous erythema excoriations - scratch marks (suggests itchy) lichenification - skin thickening in response to chronic scratching/rubbing atopic ezcema
37
what is atopic ezcema what causes it when does it present
intensely pruritic (itchy) chronic inflammatory condition Complex genetic disease with environmental influences Typically begins during infancy or early childhood
38
39
what other conditions are often closely associated with atopic ezcema
other atopic disorders: asthma rhinoconjunctivitis - hayfever
40
how does atopic ezcema present
infants - acute inflammation of cheeks, scalp and extensors children and adults - flexural (in skin creases) inflammation and lichenification
41
what is dermatitis
umbrella term for ezcema: different types of ezcema - atopic eczema, seborrhoiec dermatitis, venous stasis eczema, allergic contact dermatitis, irritant contact dermatitis
42
how is atopic ezcema managed
daily emollients and anti-inflammatory therapy
43
what essential characteristic is needed to diagnose atopic eczema
inflammed areas need to be itchy
44
what is the pathophysiology of ezcema
defective barrier and immune dysregulation process of keratinocyte differentiation (progressing from basal to stratum corneum layer) needs filaggrin filaggrin binds and aggregates keratin bundles and intermediate filaments to form the cellular scaffold in corneocytes (top layer) loss of function mutation in filaggrin gene in people with atopic ezcema so stratum corneum does not form properly so does not function as a barrier (makes you predisposed to ezcema) also there are reduced extracellular lipids and impaired ceramide production overal effect is increased transepidermal water loss and impaired barrier means you have less protection against microbes and environmental allergens Staphyloccocuss aureus finds the abnormal skin very hospitable Staphylococcal superantigens stimulate Th2 lymphocyte responses and subvert T‐reg cells Eosinophils are also stimulated
45
what is the main immune cell involved in atopic eczema
Th2
46
how does atopic ezcema present in infants
erythematous, oedematous papule (small raised areas) & plaques (larger raised areas) vesiculation - small blisters but they are scratched very quickly
47
how does ezcema present in children and adults
lichenification - thickening of skin in response to chronic scratching (excoriation) exaggeration of normal skin markings disordered pigmentation flexural location of the atopic ezcema (in creases of skin)
48
what clinical feature does trans epidermal water loss cause in atopic eczema
fissuring - skin cracking/splitting as epidermis is less hydrated it becomes less flexible very painful
49
what type of eczema/dermatitis is shown here
allergic contact eczema/dermatitis 4 can get it without having atopic eczema, but sometimes you can have allergic contact dermatitis on top of having atopic dermatitis
50
what is shown in this picture what causes it
impetiginisation a complication of eczema superficial infection of eczema caused by staphylococcus aureus characterised by gold crust forming
51
what condition is shown here
venous stasis eczema when legs are swollen keratinocytes no longer adhere to each other ⇒ barrier function of skin is lost eczema develops
52
what is shown here
ezcema herpeticum characterized by punched out erosions - a complication of atopic ezcema due to immune dysregulation caused by atopic eczema - HSV spreads very quickly erosions - breaches in the epidermis that do not penetrate all the way through the epidermis (if they went all the way through they would ulcers) manomorphic - same size in all patients needs to be treated urgently as can develop into encephalitis which can be fatal (if mistaken for atopic eczema that has just flared up and treated with steroids condition will get worse
53
what is the management of atopic eczema
**lifestyle:** Emollients - moisturize x3 daily Omission of soap Clinical Nurse Specialist involvement to terach proper Topical application technique of moisturiser and creams – gentle downward streak habit reversal - train people to recognise when they are scratching without realising it (as its a habit) **co-morbidities:** some overlap between asthma and eczema treatment **patch testing:** allergic contact eczema can aggravate atopic eczema so do patch testing to identify potential allergens **biopsy:** only done if nipple eczema does not respond to treatment and to rule out skin lymphoma
54
when is a biopsy done with atopic eczema why
biopsy is done of nipple eczema that does not respond to treatment as Paget's disease of the nipple is associated with underlying breast cancer and it presents exactly the same as nipple eczema also to rule out skin lymphoma
55
what are the treatments of eczema
Therapeutic ladder **Topical therapies:** Emolients – to support skin barrier Topical corticosteroids - correct potency for correct site Topical tacrolimus / pimecrolimus – t cell inhibitor (known as calcineurin inhibitors) **Phototherapy:** Narrowband UVB PUVA - only for hand dermatitis
56
what are the problems associated with topical corticosteroids and calcineurin inhibitors for eczema treatment how are these solved
they both very important in eczema management/treatment underuse - causes poor adherence as they don't see the beneficial effects overuse - tachyphylaxis and adverse effects **adverse effects corticosteroids:** Rare: skin atrophy (skin thinning), 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 – usually improves with time, don’t apply on broken skin **counselling is needed to teach about:** using correct steroid for correct site potential adverse effects the importance of steroid ladder (not about % dilution its about chemical structure) correct amount to use - fingerprint unit for surface of skin of 2 palms
57
what are the 2nd and 3rd line eczema treatments
58
why is it important to know about co-morbities when treating atopic eczema
biologics treatment - dupilumab which inhibits IL-13 and IL-4alpha is also used to treat asthma

BRS - Dermatology (2 decks)

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