Intro to Derm Part 2 Flashcards
what are the functions of the hair
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
what are the different types of hair
where are they
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.
what is the hair cycle
how long does hair stay in each phase
how much of our hair is in each phase
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
what is a pilosebaceous unit
what makes up pilosebaceous unit
hair shaft, hair follicle, arrector pili muscles, sebaceous gland
what are hair follicles
epidermal invagination which projects into the dermis
envelops small papilla of dermis at the base
what is the structural difference between eccrine and apocirne sweat glands
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
what is the arrector pili
where is it
what does it do
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
label this diagram
how is the hair follicle divided
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
what type of secretion do sebaceous glands carry out
holocrine
what is the bulge
what is its function
segment of the outer root sheath - located at the insertion of the arrector pili muscle
hair follicle stem cells reside here
how do hair follicle stem cells work
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
what is the bulb of the hair follicle
lowermost portion of the hair follicle
includes follicular dermal papilla and hair matrix
what is the outer root sheath of the hair follicle
where is it
reservoir of stem cells
extends along from the hair bulb to the infundibulum
what is the function of the inner sheath of the heair follicle
what is its structure
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)
what are the functions of the nails
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
label the structure of the nail
how is the nail plate produced
what is its structure
what is its growth rate
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
what is the nail matrix
where is it
what happens there
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
what is the lunula
only visible portion of the nail matrix
what is shown in these pictures
what has caused this
redness - due to inflammation
white scale - keratin
scaly red erythamatous plaques
caused by psoriasis
what is psoriasis
how do people get it
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)
what are the characterisitics of psoriasis
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)
describe the pathophysiology of psoriasis
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
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
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
what condition is show here
what can cuase it to develop
guttate psoriasis
tear drops plaques
classically follows streptococcal throat infection
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
what is the first line treatment for psoriasis
what are the second line treatments for psoriasis
what are the 3rd line psoriasis treatments
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
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
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
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)
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
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
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
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
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
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
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
what are the 2nd and 3rd line eczema treatments
