Hair Flashcards

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1
Q

Androgenetic alopecia pathogenesis

A
  • Genetics:
    • high concordance in monozygotic twins
    • Genetic loci - encodes androgen receptor oestrogen receptor-beta –> aromatase which converts testosterone to oestradiol
    • WNT signalling pathway
  • Hormones
    • androgens initiate, and inhibition of these will arrest progression and partially reverse hair miniaturization
    • Males:
      • testosterone converted to DHT by 5alpha-reductase (three isoenzymes of these, Type 2 predominantly in scalp and beard, as well as liver and prostate, and type 3 is epidermis and dermis)
      • genetic absence of type 2 5alpha reductase prevents development of AGA
      • In AGA: DHT and 5alpha-reductase are increased
      • DHT responsible for miniaturised hair follicles and hair shafts
    • Women:
      • family history
      • peri-menopausal and menopause
    • Children:
      • prepubertal
      • strong family history
      • no evidence for testosterone/precocious puberty
    • Increases prostaglandin D2 synthetase as well
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2
Q

Androgenetic alopecia male clinical

A
  • frontoparietal and frontal recession

- assess via Hamilton or Norwood system

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3
Q

Androgenetic alopecia female clinical

A
  • diffuse central thinning of the crown with preservation of the frontal hairline
  • ‘Christmas tree’ - frontal accenutation of the hair loss
  • history of increased hair shedding may precede the clinical appearance
  • Assess with Sinclair scale 1-5
    • 1 is normal
    • 2 - widening of central part line
    • 3- widening of the part line with translucency of the hairs at its border
    • 4- bald area anteirorly along the part line
    • 5 - advanced hair loss
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4
Q

Androgenetic alopecia histology

A
  • Scalp hairs exist as follicular units composed of 3-5 shaft-producing follicles serviced by a single arrector pili muscle
  • As follicles miniaturise, follicular units produce only 1-2 terminal hairs
  • once all follicles miniaturise, then baldness is observed
  • Normal total number of follicles
  • Increased number and % of vellus hairs
  • Numerous fibrous streamers
  • Increased telogen count
  • Uninvolved scalp appears normal
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5
Q

Androgenetic alopecia treatment male

A
  • Topical minoxidil
    • biologic modifier
    • 1 ml BD
    • Adverse effects: dryness, irritation, ACD
    • Initially have shedding of telogen hairs and paradoxical worsening of hairs in first 4-6 weeks
  • Oral finasteride
    • 1 mg daily
    • Type 2 5alpha-reductase inhibitor
    • halts hair loss in 90% of patients, and partial regrowth in 65%
    • halting medication results in resumption of hair loss
    • A/E: loss of libido, reduced ejaculate, erectile dysfunction ~2%
    • Prostate cancer reduced, but high dose may increase risk ?unsure if due to extra screening or truly causes
    • can affect PSA, adjust PSA by 40-50% more
  • Surgical hair replacement
  • Oral PGD2 receptor antagonist - setipiprant
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6
Q

Androgenetic alopecia treatment female

A
  • topical minoxidil
    • low to moderate level of evidence
  • Oral contraceptive
  • Spironolactone
    • if fall pregnant on this, feminization of male featus
  • Finasteride
    • not helpful in post menopausal women
  • Dutasteride
    • Type 1 and 2 5alpha-reductase inhibitor
    • teratogenicity though so not ideal for childbearing women
    • may be more effective than finasteride
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7
Q

Androgenetic alopecia trichoscopy

A

peri-pilar brown halo, miniaturisation

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8
Q

Telogen effluvium background

A
  • normal scalp: ~100 000 hair follicles, 90% in anagen phase and 10% telogen
  • Telogen lasts for 3 months
  • Daily - 50-200 hairs undergo exogen and shed, and 500-1000 are in transitional catagen phase
  • Anagen: hair will grow for a few months-years, then becomes telogen and sheds
  • Telogen effluvium is when an abnormally large numbers of hairs
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9
Q

Telogen effluvium pathogenesis

A
  • shedding of the newborn or postpartum
  • Chronic telogen effluvium –> women 30-60 years of age, dx of exclusion
  • Postfebrile
  • Severe infection
  • Severe chronic illness
  • Stress
  • Postsurgical
  • Hypothryoidism and other endocrinopathies
  • Crash or liquid protein diets
  • Drugs
    • Discontinuation of OCP
    • Retinoids and vitamin A excess
    • Anticoagulants - heparin
    • Antithyroid
    • Anticonvulsants
    • Interferon alpha 2b
    • Heavy metals
    • Beta blockers
  • Hair loss begins 3 months after defining event - amount of time that it takes to progress through telogen phase and then be shed
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10
Q

Telogen effluvium clinical

A
  • Thinning of the hair
  • Hair pull - positive for 2 or more telogen hairs
  • Forcible pluck - mixture of anagen and telogen, with telogen >20%
  • Diagnostic: telogen hairs >20%
  • 60 second timed hair count:
    • brush hair for 60 seconds over a cloth of a contrasting colour
    • usually in excess of 100 hairs
  • Prognosis: hair regrowth is expected
  • If cause unclear - thyroid, chemistry, FBC, ferritin –> ferritin should be at least 40
  • If >6 months - scalp biopsy with horizontal sectioning
  • Trichoscopy: hair shafts are of equal diameter
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11
Q

Alopecia areata epi

A
  • 0.1-0.2%
  • overall lifetime risk is 1.7%
  • 1/5 report family history
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12
Q

Alopecia areata pathogenesis

A
  • Genetics
    • regulatory T cells
    • HLA alleles, IL-2, IL-21 etc
  • Immune
    • CD8 T cells initial intrafollicular lymphocytes to appear in alopecia areata
    • Involvement of interferon gamma - downstream signaling via the JAK pathway
  • Autoimmune
    • autoantigen from melanocytes which are active during the anagen
  • Associated conditions
    • Atopy
    • Autoimmune thyroid disease, vitiligo, inflammatory bowel disease
    • Autoimmune polyendocrinopathy syndrome type 1
    • Type 1 diabetes
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13
Q

Alopecia areata clinical

A
  • Round or oval patches of non-scarring hair loss
  • Short exclamation point hairs - particularly at margins of areas of alopecia
  • Alopecia totalis: loss of all scalp hair
  • Alopecia universalis: scalp and body hair
  • Ophiasis: band like pattern of hair loss along the periphery of the temporal and occipital scalp
  • Beard involvement
  • Reticular variant: recurrent, patchy disease in which the patient experiences hair loss in one area while regrowing in another
  • Diffuse variant - widespread thinning, primarily affects the top of the head, white hairs aren’t affected so think they’re going gray. Regrowth may initially be depigmented and then pigment
  • Extra-cutaneous:
    • Nail pitting
    • Trachyonychia
    • Brittle nails
    • Onycholysis
    • Koilonychia
    • Onychomadesis
  • Dermoscopy: yellow dots in follicular ostium of empty and hair-bearing follicles, exclamation point hairs
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14
Q

Alopecia areata histology

A
  • Early:
    • normal total number of hairs
    • peribulbar mononuclear cell infiltrate, affecting terminal anagen and catagen bulbs –> ‘swarm of bees’
    • some inflam exocytosis into bulbar epithelium
    • increased numbers of terminal catagen and telogen hairs
    • increased number of miniaturized hairs
    • trichomalacia
  • Chronic:
    • majority of hairs in catagen or telogen phases
    • numerous miniaturised arrest rapidly cycling hairs - ‘nanogen’
    • mild peribulbar infiltrate
    • Fibrous tracts extending along site of previous follicles in the subcutis
    • Inversion anagen:telogen ratio
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15
Q

Alopecia areata treatment

A
  • topical: steroids, minoxidil, anthralin, azelaic acid, immunotherapy (DCP)
  • Intralesional steroids - 2.5-5 mg/ml, repeat every 4-8 weeks, inject at level of mid dermis to target the diseased hair bulbs
  • Systemic steroids - pulsed dosing –> 80% respond to his, however 50% relapse with dose reduction or cessation of therapy
  • JAK inhibitor: tofacitinib, ruxolitinib
  • PUVA
  • Excimer laser
  • Long term steroids
  • Systemic cyclosporin
  • Cosmetic
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16
Q

Alopecia areata ddx

A
  • Tinea capitis
  • Trichotillomania
  • Temporal triangular alopecia
  • Traction alopecia
  • Secondary syphilis
  • Loose anagen syndrome
  • Pressure related alopecia
  • Aplasia cutis
  • Cicatricial alopecia thats burnt out
17
Q

DCP in alopecia areata

A
  • sensitize with a 2% acetone to a 4X4 cm area on one side of the scalp
  • after 1 week –> apply 0.001%
    • sensitizer left on for 48 hours then washed off
    • shouldnt touch for 6 hours
    • scalp should be protected from light
  • each week, apply DCP or Squaric acid to same side of the scalp - the concentration is titrated according to the severity of the reaction - you want to maintain a low grade, degree of erythema, scaling and pruritus
  • eventually bring up to 2
  • once hair growth is established, then do the other side
  • takes 12 weeks to see response
  • A/E: lymphadenopathy, eczema, PIH
  • CI: pregnancy, malignancy and blood dyscrasias