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71 Cards in this Set

  • Front
  • Back
hair type:
– Androgen dependent
– Thick, pigmented
– Beard axilla, pubic areas
– no terminal hairs until puberty
terminal hairs
hair type:
– Fine hairs (peach fuzz)
– Newborns
lanugo hairs
hair type:
– Androgen independent
– Short, fine, non-pigmented (generally)
– Covers body
vellus hairs
• In a normal healthy person's scalp about 90-95% of the hair follicles are actively growing hair and 5-10% are resting.
• A hair follicle usually grows on the scalp for 2-6 years.
• Eyebrows and eyelashes grow on average 1-6 months.
• _________ or transitional phase is about 2-3 weeks.
• ________ phase on the scalp averages 2-3 months, but is longer for eyebrows and eyelashes.
• most concerned with ________ phase in hair loss
catagen
telogen
telogen
"resting, to flow out"
Precipitating stressor that leads to shift to up to 50% of telogen hairs or resting phase.
Presents with increased diffuse shedding of hair and eventual widened part.
-temporal areas and crown will more likely be pattern baldness
Shedding lasts about 2-4 months with a recovery period of 4-9 months.
-hair will come back, no scarring, more common in adults, more common in females
No scarring or inflammation is noted.
Occurs at any age, more common in adults
More common in females
telogen effluvium
Precipitating stress can include:
Illness
Operation
Accident
Childbirth
Emotional trauma
Weight loss or unusual crash diet
Oral contraceptive pill
also accutane
telogen effluvium
History & Physical
Sudden vs gradual loss
Localized vs generalized loss
Duration of hair loss
less than a year from the stressor
Medications
oral contraceptives, accutane
Severe diet restriction
Vitamin A supplements
Thyroid symptoms
hypothyroid
Recent illness
Family history of hair loss
family history in pattern baldness
Scarring vs non-scarring alopecia on exam
Hair density/part width
Hair pull test (< 6 hairs per pull)
> 6 is abnormal
Daily counts (between 100-250)
(normal hair loss is between 100 - 250 a day)
Labs: CBC, serum ferritin (tells what iron stores are like, anything less than 100 needs iron supplementation, ferritin > 30 person can make blood ok but probably not high enough to make good hair)
thyroid, Hb, Hct
telogen effluvium
Treatment : Reassurance hair will regrow
Ensure healthy diet to promote hair growth
Cosmetic ways to make hair look thicker
Minoxidil
(shifts hairs back into anagen phase, stops some of shedding until normal growth returns)
telogen effluvium
• Loss of hair in growth phase
• (usually patients in chemotherapy, hair comes out in patches)
• Abrupt insult from cancer chemotherapeutic agents and radiation therapy to the metabolic and follicular reproductive apparatus
• Once therapy is discontiued, hair will regrow.
• Doesn't necessarily come back the same: color, texture, thickness, etc
anagen effluvium
• Male pattern
Pt profile:
family history
Onset 12 – 40 years of age
Morphology
Two follicle types
Top: androgen sensitive
will lose hair in androgen sensitive areas
Sides/back: androgen independent
In the presence of androgens, terminal hairs are replaced by vellus hairs
androgenic alopecia
• Management
2 - 5% minoxidil (topical)
Dizziness and tachycardia have been reported
30% stop losing more hair, 30% regrow and 30-40% don’t respond
(have to keep using, otherwise hair loss returns at accelerated rate)
side effects: hirsutism on face, others:
Propecia (oral)
originally for BPH
Inhibits 5 alpha-reductase Type II
6-12 months for results
No significant results in post-menopausal women
($60 per Rx)
20-30% of men don’t respond
4% sexual dysfunction
(retrograde ejaculation)
Cannot be used in women with child-bearing potential
(off label in post menopausal)
(blocks all testosterone in fetus)
adrogenic allopecia
• Female pattern
Pt profile
Family history
Morphology:
Loss on vertex
Not as complete as male
More likely to include entire scalp
(mostly androgen independent)
Etiology:
Usually begins at menopause
Drop in estrogens-relative increase in androgens
adrogenic allopecia
female
• Management
Same as telogen effluvium
Draw DHEAS levels (androgen in women)
Total serum testosterone-normal in female thinning
Serum prolactin (can cause marked hair loss)
CBC, serum ferritin

telogen effluvium tx:
Reassurance hair will regrow
Ensure healthy diet to promote hair growth
Cosmetic ways to make hair look thicker
Minoxidil
(shifts hairs back into anagen phase, stops some of shedding until normal growth returns)
adrogenic allopecia
female
• Sudden/localized/generalized/ universal hair loss in discrete, round or oval areas
• Clinical findings:
< 25 years of age
Family history
No inflammation, tenderness or adenopathy
Minimal erythema if any
Exclamation point hairs
hair thins toward scalp
alopecia areata
exclamation point hairs
alopecia areata
• Diagnosis:
Clinical findings:
Perform Serum iron,
Thyroid profile,
ANA,
KOH prep to R/O other causes
• used when loss localized to scalp or facial hair or body hair
(not all three)
• Alopecia totalis used when loss is on the scalp and facial hair
• Alopecia universalis used when loss is throughout the entire scalp, face and body
• Loss in the temporal and occipital areas is referred to as the ophiasis pattern
(makes prognosis worse)
-autoimmune disorder
alopecia areata
• Management
Trial of Class I topical or intralesional steroids
Anthralin (causes contact dermatitis, causes burning and gradually increase time and hope is that WBC attack but leave hair follicles alone)
Topical immunomodulators such as Tacrolimus, Pimecrolimus
Topical or oral PUVA
IM/Oral steroids
alopecia areata

• Management
Trial of Class I topical or intralesional steroids
Anthralin (causes contact dermatitis, causes burning and gradually increase time and hope is that WBC attack but leave hair follicles alone)
Topical immunomodulators such as Tacrolimus, Pimecrolimus
Topical or oral PUVA
IM/Oral steroids
• Prognosis
The older the patient, the better the prognosis
Worse if totalis, universalis or ophiasis pattern
• Regrowth
Starts as vellus hairs which progress to terminal hairs
(they will be blonde)
• Differential diagnosis
Tinea capitis especially in kids
(won't be primary in adults, consider other ddx)
Secondary syphilis is scalp has moth-eaten appearance
alopecia areata
• Pt profile
tight braiding of hair, pony tails, hot comb straightening or rollers
• Morphology
fracture of shaft due to traction
follicle can be damaged or destroyed
receding hair line
• Treatment
no tension
Traction Alopecia
• Hair twisted around finger and pulled out or rubbed until broken off
(anxiety disorder)
• Patient obtains pleasure, gratification or relief with recurrent pulling out of hair
• Prevalence 0.6 –13%
• Young children, adolescents and females with an onset generally around 11-13 years of age
Trichotillomania
• Scalp, eyebrows, eyelashes
• Irregular, angulated border (used to distiguish it from other disorders)
• Hair density is decreased but the area is not bald
• Comorbid mood or anxiety disorder
• Skin biopsy is often warranted
Trichotillomania
• Findings:
Hair loss on crown/vertex
Progressive disease with eventual burnout
Symmetrical expansion
Most active disease at the periphery
Cicatricial Alopecia (Irreversible Hair Loss)

a scarring alopecia
• Types:
Follicular degeneration syndrome –
generally seen in African Americans with premature desquamation of inner root sheath
Pseudopelade –
slowly progressive cicatricial alopecia without clinical evidence of folliculitis
Cicatricial Alopecia (Irreversible Hair Loss)

a scarring alopecia
types:
Folliculitis decalvans –
chronic pustular eruption of scalp resulting in patchy permanent alopecia
(Tx rifampin, clindamycin, dapsone, topical mupirocin)
Tufted folliculitis –
end-stage of folliculitis decalvans or acne keloidalis, a scarring alopecia in which multiple hair tufts emerge from dilated follicular orifices
Cicatricial Alopecia (Irreversible Hair Loss)

a scarring alopecia
Occurs on the occiput after shaving,
Predominantly in African Americans,
Tx - Topical antibiotics (Erythromycin/Clindamycin); Oral antibiotics (Tetracyclines/Erythromycin); Topical/intralesional steroids
(never cut out)
• Acne Keloidalis -

a scarring alopecia
Most often young adult, African American males,
multiple inflammatory nodules that coalesce into boggy fluctuant areas that eventually discharge purulent material, eventual fibrosis, scarring and permanent hair loss,
occurs in a triad with Hidradenitis and acne conglobata. Tx – Isotretinoin
• Dissecting Cellulitis –

a scarring alopecia
Lichen planus affected the scalp,
biopsy necessary to make the diagnosis,
Tx – plaquenil, cyclosporine
• Lichen Planopilaris –

a scarring alopecia
Women more affected than men,
atrophic areas with erythema, scaling, telangiectasias and mottled hyperpigmentation,
Follicular plugging is also common.
Biopsy is warranted.
Tx – intralesional steroids and Plaquenil
• Discoid Lupus Erythematosus –

a scarring alopecia
mature terminal hairs in male pattern on female
hirsutism
mature terminal hairs in area not usually hairy
hypertrichosis
Genetic:
PCOS (polycistic ovarian syndrome)
Racial
Familial
Physiologic:
Puberty
Pregnancy
Menopause
Endocrine:
Hypothyroidism
Acromegaly
Congenital lesions
Porphyria
Drugs:
Androgens
Diazoxide
Glucocorticoids
Minoxidil
OCPs
Phenytoin
CNS lesions:
MS
Encephalitis
• Hisutism without virilization
Ovarian
PCOS
Hyperthecosis
HAIR-AN syndrome (hyperandrogenism, insulin resistence, acanthosis nigricans)
Tumors
Adrenal
Congenital Adrenal Hyperplasias
21-hydroxylase deficiency
11-hydroxylase deficiency (rare)
3beta hydroxysteroid dehydrogenase deficiency (rare)
Tumors
ACTH-dependent Cushing’s syndrome
• Hirsutism with virilization
• Work up
Age of onset, severity, rate of progression
Virilization present or absent
Family history of similar pattern
Initial labs: DHEA-S and free and total serum testosterone
hirsutism
If virilization present:
TeBG
17-hydroxyprogesterone
LH
FSH
thyroxine
androstenedione
ovarian US
hirsutism with virilization present
Vaniqa
enzymes that inhibit hair growth
Cosmetic intervention
Shaving
Waxing
Plucking
Bleaching
Depilatories
Vaniqa (enzyme that inhibits hair growth)
Electrolysis
Lasers (only permanant form of hair loss)
OCPs (can help it, but it can also cause it)
Finasteride (DO NOT USE in women of child-bearing potential)
Spironolactone (antiandrogen, CI: pregnancy)
Flutamide (temporary chemical castration)
hirstutism
• Combination of acne, hirsutism, weight gain and infertility or irregular menses
Polycystic Ovarian Syndrome
• 6% of women of reproductive age
• Virilization generally absent
• Associated with insulin resistance
Polycystic Ovarian Syndrome
• Labs:
Elevated testosterone
elevated LH and LH:FSH ratio 3:1
elevated DHEA-S
serum prolactin
Polycystic Ovarian Syndrome
• Treatment:
weight reduction
diet and exercise
low dose OCP
spironolactone
flutamide
Clomiphene
Metformin
Polycystic Ovarian Syndrome
• over-processed hair
• Pt profile
brittle due to over working hair
small bead on hair
• Treatment
stop all hair treatments
in African Americans can cause permanent loss due to scarring
Trichorrhexis Nodosa
Longitudinal ridging
Pigmented bands
Beading
normal nail variants
• Separation of nail plate from nail bed
• Potential space for infection
Onycholysis
• Etiology:
psoriasis-pitting and oil spots
atopic eczema
candidiasis
trauma
Treatment :
Based on underlying etiology:
Psoriasis:
Intralesional steroids monthly injected into the matrix,
Calcipotriol, Tazarotene, Anthralin
Candidiasis:
Fluconazole
Onycholysis
• Rapid onset
• Red,painful area to proximal/lateral nail fold
post-trauma
usually due to Staph
mild and localized
• Treatment:
I & D, po antibiotics with penicillinase-resistant antibiotics
Acute Paronychia
• Seen in individuals whose hands are subjected to moist local environments
• Redness, edema of nail fold, several fingers, long term dystrophy of nail
• Cuticle separates from the proximal nail fold, increasing risk of infection
nail changes seen
edema but it is not purulent
Chronic Paronychia
• Treatment:
Avoid exposure to contact irritants
Keep proximal nail fold dry
use cotton liner gloves
Control inflammation with class 5 steroid
Miconazole or Thymol in ETOH placed on the proximal nail fold
Fluconazole if it appears to have candidal overgrowth
Chronic Paronychia
• Clinical findings:
Prodrome - tingling, itching, burning
Grouped vesicles on an erythematous base
Dentists and nurses high risk before advent of glove use
Regional adenopathy
Herpetic Whitlow
nearly always caused by herpes
Course - 7-10days
• Diagnosis:
History
Clinical findings
Tzanck prep
DFA
Culture
• Treatment:
Acyclovir
Viral Paronychia
• Frequent moist environments allows introduction of this bacteria
• Nail develops green-yellow or black color due to infection in areas of onycholysis
• No inflammation, little to no discomfort
• Treatment
dry area
One part chlorine bleach/4 parts water under nail TID or vinegar
Ciprofloxacin
Pseudomonas
• Also known as tinea unguium
• Generally due to Trichophyton rubrum or Trichophyton mentagrophytes
• 50% of thickened nails are not due to fungal infection
(psoriasis; need to culture - part of nail or debris under nail)
Onychomycosis
• Distal subungual ______________ – most common
Yellow or white, hyperkeratotic debris
Crumbly and fragment
Onychomycosis
a type of onychomycosis:
Surface invasion of the nail plate which is soft, dry and powdery
white superficial
Infection starts at proximal nail fold and migrate to matrix and invade nail plate
Transverse white bands begin proximally
reverse of distal subungal - starts proximally
Usually white
Most commonly seen in AIDS
• Proximal subungual onychomycosis
Thickened, yellow-brown nail plate
• Candida onychomycosis
Treatment:
KOH and culture
(need confirmatory culture: can look like psoriasis, drug coverage)
Griseofulvin (takes up to 1 year for therapy)
Itraconazole
200mg, 2 PO qd x 1 week, off for 3 weeks, total off 3 months)
RR 38.3%
Terbenifine
250 mg qd x 3 months
(can be used with children)
RR 75.5%
Fluconazole
150mg Q week x 12 – 24 weeks
RR 32%
Ciclopirox nail laquer
Used best as added agent to orals and to prevent recurrence
Surgical removal
Vicks Vapor Rub?
Onychomycosis
• Nail is severly distorted, thickened, opaque, brownish, spiralated and without attachement ot the nail bed
• Nail of the great toe is particularly vulnerable.
• Usually caused by pressure from footwear in the elderly
or DM
Onychogryphosis
• Appears during 5th or 6th decade of life
• Minimal inflammation of the matrix induces longitudinal grooving and ridging
• A pterygium caused by adhesion of the nail matrix with scarring can develop
• Treatment with intralesional TAC
• Oral prednisone in severe cases
• usually irreversible
Lichen Planus
nail:
cuased from trauma
leukonychia punctata
genetically predisposed
may have nail removed and destroy nail bed matrix to prevent regrowth of nail
pincer nails
Median Nail Dystrophy
if nail matrix injured, will have permanent ______ in nail
groove
coincide with some other issue
nails:
transverse linear depressions
illness or extreme stress
• Beau’s lines

associated with internal disease
nails:
Elderly
Pulmonary complaints
Pleural effusion, bronchiectasis bronchitis, COPD
Facial or lower extremity edema
Abnormal lymphatics
light or deep yellow
Slow growth of nails
thick and ridged
Treatment:
Vitamin E orally or topically has shown some improvement
yellow nails

associated with internal disease
nails:
look for in pulmonary disease
distal finger enlarged nail convex
May occur as a normal variant
Associated with lung/cardiac disease
Cirrhosis
Thyroid disease
clubbing

associated with internal disease
nails:
Spoon nails-central depression of nail plate
-normal variant unless anemic
-iron deficiency
koilonychia

associated with internal disease
nails:

transverse white line in plate
-sepsis
-renal failure
-arsenic poisoning
Mee's nails

associated with internal disease
nails:

proximal white distal red/brown
– associated with renal disease
Half and half nails

associated with internal disease
nails:

liver disease
Terry's nails

associated with internal disease
nails:

Azure Lunula
an autosomal recessive disorder, with a male preponderance. Its main feature is accumulation of copper in tissues, which manifests itself with neurological symptoms and liver disease
Wilson's diease

associated with internal disease
nails:
usually occurs around puberty
a rare, multi-system genetic disease that causes benign tumours to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. A combination of symptoms may include seizures, developmental delay, behavioural problems, skin abnormalities, lung and kidney disease
Koenen’s Tumors in Tuberous Sclerosis
nails:
abnormal vascular collection
benign
lots of bleeding,
may want to refer to hand surgeon
pyogenic granuloma

-nail tumor
nails:
very difficult to get rid of aldera or nevus nail
periungual wart

-nail tumors