dermatology in general medicine

1. PATIENT WITH HAIR
LOSS
PRESENTED BY : DR MANISHA CHAUHAN
MODERATOR : DR AASTHA
SUPERVISOR : DR POOJA

2. History of hairloss
•Complaints - Thinning or shedding or both
•Duration
•Onset- acute or chronic
•Pattern of hairloss- Diffuse or localized
•Associated symptoms- itching , pain , burning
•Present & medical history

3. •Drug history
•Nutritional history
•Psychological history
•History of hair care practices / use of hair
cosmetics
•Family history
•Androgen excess ( in women )

4. Age related
• Children - Alopecia areata , tinea capitis
• Prepubertal to young adult- tractional alopecia ,
trichotillomania
• Postpuberatal - Patterned hairloss ( PHL )
• Postmenopausal - frontal fibrosing alopecia

5. SCALP EXAMINATION OF NON SCARRING HAIR
LOSS
NORMAL
LOOKING SCALP
ABNORMAL
LOOKING SCALP
PSORIASIS
DIFFUSE - ANAGEN HAIRLOSS
TELOGEN HAIR LOSS
SEBORRHOEIC DERMATITIS
PATCHY - ALOPECIA AREATA,
TRIANGULAR ALOPECIA
DERMATOPHYTIC INFECTION
TRICHOTILOMANIA,
SECONDARY SYPHILIS
TRACTION ALOPECIA PHL - MAGA & FAGA

6. Alopecia
Non cicatricial alopecia Cicatricial alopecia
Localized hairloss
Diffuse hairloss
Classification of alopecia

7. EXAMINATION OF SCALP

8. Evaluation technique
Of Hair loss
Methods Technique Merits Demerits
DAILY COUNT
Pt is ask to collect hairs
for 7 days & count
If >100/day hair m/s is
performed
Provide rough estimate
of hairloss
Daily counts are tedious,
time consuming
60-s hair count
Pt. collect hair before
shampooing by
combing for 60 s from
back to front of scalp
Repeat procedure for 3
consecutive shampooing
Patient can self monitor
their progress following
therapy
Estimate of daily hair
shedding vary widely
& age specific

9. Standardized
and
modified wash
test
Pt is refrain from
shampoo for 5 days,
then do & Collect hair
shed & count and
divide <3 cm & > 5cm
Give a rough estimate
about hairloss
Very tedious
Lack of correlation
with vellus hair count
AGA - <100
hairs/day with
>10% telogen
CTE- >100
hairs/day
<10% telogen hair
AGA+CTE -
>100 hairs /day
with >10%
telogen hairs

10. HAIRPULL
TEST
( traction test /
sabouraud’s
sign)
Abstinence from
shampoo for 2-5 days
Approx. 50-60 hairs are
grasp b/w thumb
&index finger
&tugged away
Repeat in 4 section
( both parietal , frontal ,
occupital )
Merits
Give estimate of
severity of hairloss
Simple & inexpensive
test
Demerits
Difficult to
standardized the
pressure of hair pull
Light microscopepy is
essential to d/f in diff
condition
Test is positive - >10%
hairs are grasped or >6
hairs are pulled away
on scalp
Positive test
Seen in -
Acute TE
Active phase of CTE
Early case of PHL
Active edge of AA
Loose anagen phase
Active AGA - test is
positive on top &
negative on occiput

11. Trichogram /
Hair pluck
test/
Unit area
trichogram
Abstinence for
shampoo for 5 days
Use rubber forceps,
60-80 hairs pluck at 2
specifyic sites for
AGA
Hair grasp 0.5 cm
from scalp &
removed along
direction of hair
growth
Examine under
microscope
Cut shaft of TG
examined under
polarized microscopy
UAT >> TG
Highly effective
knowing hair density,
diameter
Painful for the pt
Inappropriately
perform cause
dystrophic bulb &
broken hair
Method to
evaluate hair
root & hair
cycle
Results are expressed
as A:T
Normal - 14:1
CTE- 8:1
Merits Demerits

12. PHOTO
TRICHOGRAM
Day 0- hair in a selected area
1cm are cut closet scalp
Vertex is selected in MAGA
Midscalp is used in
FAGA
Hair is mounted & diameter of
clipped hair measure under 40x
microscope
Marked area is photographed
Non invasive test
Measure hair growth cycle,
hair density , linear hair
growth rate, hair thickness
Day 2- second photography
after 48 hrs
Hair variable on
Day 0- density & length of hair
Day 2- no. of hairs growing
shows (anagen hair)

13. TRICHOSCAN
Its a method of in vivo hair growth that combines
epiluminescence microscopy with automated digital
image analysis.
Calculate a digital PTG within 15 min
HPE
Recommend only in cases with telogen loss lasting for 6
months
4mm biopsy taken from vertex & horizontally
ATE- Absent follicular miniaturization & perillbulbar
lymphocytic infillrate
CTE- INCREASE in telogen hair
A:T - 8:1 ( normal - 14:1)
AGA - T:V - 1.9:1 (normal - 7:1)

14. Hair break with roots Hair break without root
Telogen effluvium Tinea capitis
Alopecia areata Trichotillomania
PHL
Improper hair care practices/ haircare
cosmetics
DRUGS Structural hairshaft disorders
Loose anagen hairs Anagen effluvium

15. Localized hair loss Diffuse hair loss
Alopecia areata
Trichotillomania
Loose anagen syndrome
Tractional alopecia
AG
A
Telogen effluvium
Chronic diffuse telogen hairloss
Chronic telogen effluvium
Hairshaft disorders
Syphilitic alopecia
Tinea capitis
On the Basis of Extent

16. Telogen effluvium
• The term was coined by Kligman in 1961
• An increase shedding in the telogen club hairs due to premature
termination of anagen phase of the cycle
• Follicles is precipitating into catagen transform into resting
stage that mimics telogen
• Normally, Anagen - 86% , catagen - 1% , telogen -13%
• In TE, Anagen- 70% and telogen become 30%, with daily
shedding of unto 300 hairs

17. TELOGEN
EFFLUVIUM
ACUTE
TE
( 2-4 months )
CHRONIC
TE
( Idiopathic pattern )
CDTHL
(Secondary to identifiable
Cause )

18. Etiopathogenesis
• The normal hair cycle consists of anagen( growth phase),
catagen (involution), telogen ( dormant phase ), exogen (
release phase )
• Telogen hair remains in follicles for 4-6 weeks after onset of
anagen
• This cycle replace every hair on scalp every 3-5 year with
Individual follicle undergoing 10-30 cycle
• In humans , synchronous hair growth disappears in childhood

19. • Headington described five functional types of TE -
IMMEDIATE
ANAGEN RELEASE
( Stress, illness,
drug induced)
SHORT
ANAGEN RELEASE
(CTE & AGA)
DELAYED
ANAGEN RELEASE
(Telogen gravidarum )
IMMEDIATE
TELOGEN RELEASE
Premature removal of
Mature hair follicle
( therapy with minoxidil )
DELAYED
TELOGEN RELEASE
(Animals with
synchronous hair cycle)

20. Physical & emotional stress
Postpartum
Shedding in newborn
Post surgical , psychological, crash dieting, seasonal
variation , UV induced
Disease
Severe infection
High fever
Endocrine causes
Hyperthyroidism, Hypothyroidism , hypoPTH,
Hypopituitarism , hyperandrenocortism,
Diabetes, Cushing syndrome
Acromegaly, hyperprolactenemia
Dermatitis
ACD to hair dye
( paraphenylenediamine)
Etiology of TE

21. DRUGS
RETINOIDS ( ETRETINATE > ACITRETIN )
CYTOTOXIC DRUGS,
ANTIHYPERTENSIVE ( b blocker, ACE
inhibitors ) , heavy metals ( thallium ,arsenic)
Heavy metals ( thallium, arsenic, lead )
ANTICONVULSANT (PHENYTOIN,
VALPROATE )
ANTICOAGULANTS,
MINOXIDIL,
Discontinuation of oral contraceptives
Alopecia areata with slow
progression
Androgenetic alopecia Patient of CTE may overlap with FAGA
Psychogenic pesodoeffluvium

22. Acute TE
• TRIGGER FACTOR generally precedes excessive hairloss by
2-4 months
• Sudden baldness over temples ( symm bitemporal thinning)
• Hairloss is less than 50%
• Factors - physiological stress , inadequate diet, hemorrhage
,shock, acute iron deficiency
• Postpartum TE, persistent TE, seasonal hairloss

23. Chronic diffuse telogen hair loss
•Refer to the hair shedding longer than 6 months, secondary to
organic causes or coexist with FAGA.
•When no triggering factor of chronic telogen loss is found
labelled as CTE ( coexist with AGA )
• O/E-
• Bitemporal thinning
• Positive hair pull test ( vertex= occiput )
•No widening in central part ( commonly seen in AGA)
•Mechanism - SYNCHRONIZATION of hair cycling, shortens
anagen phase , premature teloptosis

24. • Causes -
• Endocrine causes-
• Hyperthyroidism, Hypothyroidism , hypoPTH, Hypopituitarism ,
hyperandrenocortism, Diabetes, Cushing syndrome ,
hyperprolactenemia
• Metabolic & nutritional causes-
• Vit D , FERRITIN , ZINC DEFICIENCY plays imp role
• S . Ferritin - <30 microgram/dl precipitate telogen hairloss
• Nutritional deficiencies - a/w dieting, malabsorption , parenteral
nutrition

25. • Rare causes -
• SLE - cause frontal , non scarring hair loss and thinning
• Secondary syphilis - patchy alopecia ( bald patches over
temporoparietal areas )
• External/ traumatic - frequent bushing, hairstyling
• Psychological causes
• Idiopathic (33%)

27. CHRONIC TE
• It can result of an idiopathic change in hair cycle ( primary
CTE ) OR secondary to causes including FPHL
• Affecting middle age women 30-50 yrs
• Sudden onset of increase in hair shedding persist for at least 6
months
• No visible widening of central parting line, no miniaturization
of hair follicle
• Trichodynia or scalp dysaesthesia +/-

28. HAIR PULL TEST
POSITIVE (10% of hairs are pulled from occiput &
midscalp area )
Hair count test
Daily hair count
Standardized wash test
60 -s- hair test
HAIR SHEDDING OF > 100hairs/day
If <10% hairs are of 3cm - CTE
If >10% hairs are of 3cm OR more - CTE with FPHL
TRICHOSCOPY
Decrease in hair density and empty follicle
Numerous regrowing hairs +
Trichogram/ hair pluck test ATE - >25% hairs are in TELOGEN phase
Phototrichogram
Helps in assess anagen to telogen hair
( 8:1)
Scalp biopsy >25 % telogen follicles + = suggestive of TE

29. APPROACH TO INVESTIGATE
HAIRLOSS
INCREASE
HAIR
SHEDDING
DIFFUSE
HAIRLO
SS
S. FERRITIN - <30microgm/dl
Vit B12 - <200
HYPOTHYROIDISM
FREE
ANDROGEN INDEX >5
PROLACTIN >100
AMH - 2-7
( in case of hyperandrogegism )

30. • DIFFERENTIAL DIAGNOSIS-
• AGA
• DIFFUSE AA
• ANAGEN EFFLUVIUM
• LOOSE ANAGEN SYNDROME
• STRUCTURE HAIR DISORDER
• PSYCHOGENIC PSEUDOEFFLUVIUM

31. TREATMENT
• Reassurance and counseling
• Attempts at identifying specific cause
• Potential therapeutic option like -
• Inhibitition of catagen ( prolong anagen phase )
• Induction of anagen in telogen effluvium
• Inhibition of exogen ( to reduce hair shaft shedding )
• Neither of the currently available FDA approved standard hair drug

32. • Correction of the catagen inducing endocrine disorders
(thyroid disorders, hyperandrogenism, hyperprolactenemia)
• Substitution therapy for catagen promoting deficiencies like
iron, zinc, protein can also be initiated
• Balanced diet and maintaining standard body weight is imp
factors
• It is suggested that maintaining S. Ferritin above 40ng/dl helps
reversing hair loss

33. Management of TE
TOPICAL
MINOXIDIL
( 2% OR 5%)
TOPICAL
AGENTS
DIETARY
SUPPLEMENTS
REASSURANCE AND COUNSELING OF THE
PATIENT
IRON - 300mg tds
(60 mg elemental iron /day)
For 3-6 months
Millet extracts , pantothenic acid,
Biotin, CYP COMPLEX

34. Androgenetic
Alopecia
• The term ‘pattern hair loss’ describe
hairloss in distinctive pattern by
progressive declining in hair fibre
production & eventual miniaturization
• Polygenic inheritance ( mutation in
ANDROGEN RECEPTOR gene)
• PHL IN MEN - AGA
• PHL IN female - Female AGA/FPHL
• It depends on genetic predisposition
&interaction of endocrine factors

35. • Decrease in size & activity of hair
follicle during successive hair cycle
called miniaturization
• Terminal thick , pigmented hair follicles
turns to thinner ,shorter , less pigmented
till they change to vellus hair
• Anagen duration - decreased
• Telogen- constant /prolonged
• Testosterone DHT
• Binding of DHT to its receptor in hair
follicle lead to production of cytokines -
TGF B1 & B2 promote senescence
5 alpha
reductase

36. • Density of these receptors are more in
frontoparietal scalp & vertex and less
in occiput
• PG-D2 shows inhibitory effect in hair
growth( elevated in scalp of men with
AGA )

37. Decrease in hair density
Variation in hair thickness
Decrease of hair per FHU

38. Norwood- Hamilton
Classification
( MALE PATTERN CLASSIFICATION )

39. Investigation
• Change of anagen to telogen ratio from
12:1 to 5:1
• Ratio of terminal to vellus hair(
greater than 8:1 to less than 4:1)
• Proportion of telogen hairs is increased
from 5-10% to 15-20 %
• No. Of hair follicle in FHU is reduced
from 2-5 (normal) to 1-2 hair
• On dermoscopy- diversity in hairshaft
diameter>20% in frontoparietal area

40. Peripilar sign
(Brown halo reflecting
perifollicular inflammation)
Yellow dot
( sebum & keratin
accumulation with dilated
follicular infundibulum)
Increase in % of
single hair follicular
units

41. Female pattern
hairloss
• PHL in a women was first described
by Ludwig in 1977
• Present with diffuse thinning ( loss of
hair volume ) over mid-frontal scalp
with minimum or no bitemporal
recession
• Ludwig graded FPHL into 3 grades
• Genetic predisposition & polygenic
inheritance
• Shorter the length of CAG repeats in
AR gene lead to significant risk of
FPHL

42. • Stage I is characterized by a perceptible thinning of hair
from the anterior part of the crown with minimal widening
(rarefaction) of the part width .
• The hair loss at this stage can easily be camouflaged.
• This type may manifest in young women with SAHA
syndrome (seborrhea, acne, hirsutism, and alopecia),
generally of ovarian origin.
• It may be accompanied by other manifestations of
hyperandrogenism (seborrhoea, acne, hirsutism, seborrheic
dermatitis, and slight menstrual alterations)
• Biochemical levels are often normal

43. • Stage II is seen with advancing age when
the rarefaction on the crown becomes more
pronounced, and the number of thinner and
shorter hairs increases
• Camouflage of the denuded areas by
special hair styles is no longer possible.
• An excess of androstenedione, free T, and
androstanediol glucuronide may be
detectable

44. • Stage III is usually not encountered before
menopause, and the crown may become literally
bald
• Contrary to what happens in men, a fringe of hair
along the frontal hair line persists.
• Adrenal diseases, tumoral or not, with very high
levels of androstenedione, dehydroepiandrosterone
sulfates (DHEA-S), free T, sometimes of prolactin,
and always of androstanediol glucuronide

45. Normal
Hair density
Widening
of central part
Additional
Thinning of hair
At sides
of part line Bald
Patch distal
To
Hairline
Advanced
Hairloss
Sinclair scale
5 visually distinct STAGES

46. Pathophysiology
• FAGA can be related to excess of androstenedione serum level of
ovaries or adrenal
• androstenedione and DHEAS transformed into testosterone 7
convert into 5 alpha DHT mediated by 5alpha reductase
• Conversion of testosterone to DHT requires free testosterone,
highlight the importance of SHBG and free androgen
• DHT metabolized into 3 a - androstanediol glucoronide(most
sensitive marker of peripheral hyperdrogenemia
• Hyperprolactenemia is associated with increase in DHEAS

47. Basic test Full blood count
IRON PROFILE
S. VIT B12 , VIT D
Thyroid function test
Fasting lipids/ fasting glucose
Endocrine test S. Testosterone/ free androgen index
DHEAS
S. Prolactin , AMH
17- hydroxyprogesterone
USG ABDOMEN
INVESTIGATIONS

48. DIFFERENTIAL DIAGNOSIS OF FPHL
CT
E
DIFFUSE
AOPECIA
AREATA
ANAGEN
EFFLUVIU
M
TRICHOTILLOMANI
A
Early acute onset
Exclamation hairs +
Yellow dots +
Dystrophic
Anagen
Hairs
Different length
Of hairs
Abrupt
Diffuse
Thinning
Trigger +
Others - hypothyroidism, SLE, Frontal fibrosing alopecia

49. FPHL CHRONIC TE
DISTRIBUTION
Central part of scalp
Preserved frontal hairline
Generalized
ONSET Gradual Abrupt with trigger
APPEARANCE Hair thinning with midline part Diffuse thinning
HAIR SHEDDING Minimal Prominent
HAIR PULL TEST Usually negative Positive
OTHER HISTORY Family history + Stress , major illness
SCALP BIOPSY T:V >4:1 T:V>8:1

51. Treatment for FPHL

52. Alopecia areata
•Non scarring alopecia
•Occur at any age ( peak incidence 2 to
4 decade )
•Involving any hair bearing areas
•Seen over scalp , in a patchy
distribution
•Other sites- eyebrows , eyelashes,
beard, thorax area
•Nail changes(10-66%)- fine nail
pitting, trachyonychia,
onychorrhexis,onycholysis ,
onychomadesis

53. • It is a T cell mediated autoimmune disease occurs in genetically
predisposed individuals & environmental factors
• Genetic lineage focus to HLA class II ( HLA-D) on
choromosome 6
• A receptor for stress induced proteins ( NKG2D) strongly
associated
• Rapid progression of hair follicle from anagen phase to catagen to
telogen phase
• Disorder affects anagen follicles with little or no inflammatory
infiltrate around isthmus of hair follicle

54. IMMUNE RESPONSE
TARG
ET
LOSS
OF
IMMUNE
PRIVILEGE
AUTOANTIG
EN
EPITOPE
Early cortical differentiation
in hair follicle
matrix epithelium
Vacuolar degeneration
of affecting Anagen follicle
Weakness of the hairshaft
(EXCLAMATION HAIR)
Reverts to telogen phase
Renter anagen phase
Not beyond iii/iv stage
Cytotoxic subset
( CD8+ NKG2D+)
Produce IFN-Y activates
IL-15 sustains CD8+ T cell
autoreactivity
Involvement of
JAK receptors
Involvement of melanin,
Melanin related protein
Keratinocyte derived Ag
Growing of white hair
After AA

55. Clinical presentation
of AA
PATTER
N
DIFFUS
E
AA
PATC
HY
OPHIASIS
INVERSUS/SISAPHO
( band like loss of hair in
Fronto
Parietal)
OPHIASIS
( band like loss of hair in
tempero ocipital
RETICULATE
(Patchy, round to oval
Hairloss)
EXTEN
T
ALOPECIA
UNIVERSALIS
(Total loss of scalp &
Body hair )
ALOPECIA
TOTALIS
(Total loss of scalp hair)
ALOPECIA
AREATA
(Partial loss of scalp hair)

56. Poor prognostic of AA
FOR WHOLE DISEASE FOR AN EPISODE
ONSET IN CHILDHOOD DURATION OF EPISODE
ASSOCIATED ENDOCRINE DISORDER
ATOPY
EXTENT OF AFFECTED AREA
PRESENCE OF AUTOIMMUNE DISEASE
(thyroiditis, LE, vitiligo, psoriasis )
C/L form- ophiasis, A totalis, A universalis
POSITIVE HISTORY OF AA Nail dystrophy

57. Test Findings
Hair pull test
Positive >6 hair
( s/o disease is active & progressive )
Trichoscopy
Exclamation hairs
YELLOW DOT
BLACK DOT
Trichogram Increase no.of dystrophic anagen hair
4mm Punch biopsy
Swarm of bees appearance
(perifollicular & intrafollicular inflammatory infillrateof
activated T cell )
Lab work up
TSH , THYROID ANTIBODY, FERRITIN,
VIT D, VIT B12
INVESTIGATIONS

61. TRICHOTILLOMANIA
• Trichotillomania (TTM) is characterized by persistent hair
pulling behavior, resulting in noticeable hair loss.
• Patients report feeling anxious before pulling their hair out and
pleasure, satisfaction, or relief after doing it
• Asymmetrical patches of alopecia, particularly in the frontal
and vertex regions.

62. • At dermoscopy, Fracture may occur at
varying lengths, resulting in black dots,
fraying hair, longitudinally split hair,
coiled hair and stretching of the shaft.
Hairs of varying lengths and short vellus hairs
may be seen in these patches
The hair pull test is negative along the edges.
flame hair, empty hair folicular Ostia ,
follicular hemorrhages, decreased hair
density , and no sign of exclamation signs

65. DIFFERENTIAL
DIAGNOSIS
• T. capitis
• Alopecia areata
• Monilethrix
• Traction alopecia
• Secondary syphilis

66. • Treatment -
• Psychotherapy, behavioral therapy, and drugs – such as
lithium salts, tricyclic antidepressants (TADs), selective
serotonin reuptake inhibitors (SSRIs), and
antipsychotics.
• Recently, N-acetylcysteine has been proposed as an
effective alter- native treatmen

67. Tinea capitis
• Tinea capitis is a superficial
fungal infection of the scalp.
• The disease is primarily caused
by dermatophytes in the
Trichophyton and Microsporum
genera that invade the hair shaft
• A single or multiple patches of
hair loss, sometimes with a
“black dot” pattern,
accompanied by inflammation,
scaling, pustules, and itching

68. • Hair roots and skin scraping were
mounted in 10% potassium hydroxide
solution.
• Slide was gently heated and
microscopically examined for spores.
• Trichoscopic findings-
• Comma shape hair, zig zag hair, black
dot hair, short broken hair, corkscrew
hair
• A therapeutic trial of anti- fungal treatment
remains an acceptable alternative.
• The treatment of choice is griseofulvin 10
- 20 mg/kg per day, with a meal, for 6 to 8

69. SYPHILITIC ALOPECIA
•Syphilitic alopecia is considered an
uncommon manifestation of secondary
syphilis.
•SA is further classified into three forms:
•1) moth-eaten, or patchy alopecia
characterized by small alopecia patches
irregularly distributed over the scalp;
•2) diffuse alopecia, characterized by a
diffuse hair loss; resembling TE
•3) mixed form (i.e., combination of
diffuse hair loss and alopecia moth-eaten
patches)

70. • Trichoscopic features—such as
tapered bended hairs,
erythematous background, diffuse
scaling and perifollicular
hyperkeratosis
• Serology - VDRL +
• Scalp biopsies - spirochetes in the
peribulbar region and penetrating into
the follicle matrix.
• Current hypothesis supporting the
pathogenesis of SA is a vasculitis of
peribulbar capillaries causing a
perifollicular lymphocytic infiltration
with scattered plasma cells that stops
the hair cell cycle
• Treatment -
• Inj benzathine penicillin G 2.4 million
units intramuscularly
Moth eaten type

71. Tapered
Bent hairs
Fine scaling
Villus hair
( periphery)
Perifollicular
Hyperkeratosis
Yellow dots +
Trichoscopic finding in syphilitic
alopecia

72. Tractional alopecia
• Traction alopecia is a form of
trauma-induced alopecia and results
from continuous excessive pulling of
hair shafts.
• Hairstyling is the most common cause
of longstanding traction and usually
results in alopecia of scalp margins
• TA most often affects the frontal and
temporal scalp.

73. structure that encircles the hair shaft placed
at the periphery of the alopecia plaque.
• It is derived from the inner and/or outer hair
root sheath cells and it develops because of
persistent hair traction
• Treatment -
• loosen hairstyle is preferred
• Avoid chemical treatment of hairs
• I/L triamcinolone can be used at
periphery
• 2% minoxidil applecation promotes hair

74. Thank you