Androgenetic alopecia (AGA) is a nonscarring progressive miniaturization of the hair follicle in genetically predisposed men and women, usually in a specific pattern distribution.
Multifactorial and polygenetic etiology.
Clinical features:
-History of hair loss is -
long standing
slowly progressing reduction of hair density, diameter
Miniaturization of hair
Diminished anagen hair and increased telogen hair
-Pattern of hair loss in male:
Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
-Pattern of hair loss in female:
Centrofrontal hair loss with preservation of frontal hair line
(Ludwig type) {figure - left}
Christmas tree pattern {figure- right}
-Family history of AGA often positive
In female
signs of hyperandrogenism should be evaluated
gynecological history
progesterone containing pills
-To exclude other causes history should be taken regarding-
Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
Hair color, cosmetics use.
Allergic contact dermatitis
Treatment:
Androgenic alopecia is naturally progressive , so main strategy is to prevent progression and increase hair density.
1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
1 mg finasteride per day prevents progression of AGA .
0.5 mg daily dutasteride is alternative.
Combination of topical minoxidil and finasteride is good option
Response evaluated after 6 months . not indicated in women. Contraindicated in pregnant and child bearing female.
3.Antiandrogen and estrogenic drugs:
Given in hyperandrogenism in female. Not indicated in male.
Spironolactone 100-200 mg daily
Cyproterone acetate can be used
4.Hair transplantation
5.Low-level laser therapy
6.Miscellaneous: low level of evidence.
Platelet rich plasma therapy and microneedling
Herbal preparations
Topical melatonin
Nutritional supplement of- biotin, copper, zinc, aminoacids, micronutrients
Biochemistry of Hair fall, A complete review of hair fall cause, Types, Current methods of treatment, Natural methods of treatment,
for more detail text see :https://iiopinion.blogspot.in/2017/01/hair-fall-scientific-way-of-treatment.html
Androgenetic alopecia (AGA) is a nonscarring progressive miniaturization of the hair follicle in genetically predisposed men and women, usually in a specific pattern distribution.
Multifactorial and polygenetic etiology.
Clinical features:
-History of hair loss is -
long standing
slowly progressing reduction of hair density, diameter
Miniaturization of hair
Diminished anagen hair and increased telogen hair
-Pattern of hair loss in male:
Hamilton- Norwood type: recession of frontal hair line, latter followed by a vertex thinning with progression until top of the scalp is completely bald.
-Pattern of hair loss in female:
Centrofrontal hair loss with preservation of frontal hair line
(Ludwig type) {figure - left}
Christmas tree pattern {figure- right}
-Family history of AGA often positive
In female
signs of hyperandrogenism should be evaluated
gynecological history
progesterone containing pills
-To exclude other causes history should be taken regarding-
Thyroid disease,
Surgery, infection in last 6months to 1 year
Drug history
Iron deficiency
Smoking
UV exposure
Hair color, cosmetics use.
Allergic contact dermatitis
Treatment:
Androgenic alopecia is naturally progressive , so main strategy is to prevent progression and increase hair density.
1.Topical minoxidil:
2% for female and 5% spray for male 1 ml twice daily or half cup foam once daily.
There is transitory telogen shedding within first 8 weeks observed.
Response should be assessed after 6 months.
If response occurs, will be continued as main stay of treatment.
2.Finasteride oral ad Dutasteride oral
1 mg finasteride per day prevents progression of AGA .
0.5 mg daily dutasteride is alternative.
Combination of topical minoxidil and finasteride is good option
Response evaluated after 6 months . not indicated in women. Contraindicated in pregnant and child bearing female.
3.Antiandrogen and estrogenic drugs:
Given in hyperandrogenism in female. Not indicated in male.
Spironolactone 100-200 mg daily
Cyproterone acetate can be used
4.Hair transplantation
5.Low-level laser therapy
6.Miscellaneous: low level of evidence.
Platelet rich plasma therapy and microneedling
Herbal preparations
Topical melatonin
Nutritional supplement of- biotin, copper, zinc, aminoacids, micronutrients
Biochemistry of Hair fall, A complete review of hair fall cause, Types, Current methods of treatment, Natural methods of treatment,
for more detail text see :https://iiopinion.blogspot.in/2017/01/hair-fall-scientific-way-of-treatment.html
• In recent years, the usefulness of trichoscopy (scalp dermoscopy) (videodermatoscopy) has been reported for diagnosing hair loss diseases. This method allows viewing of the hair and scalp at X20 to X160 magnifications. Characteristic trichoscopy features of alopecia areata are black dots, tapering hairs (exclamation mark hairs), broken hairs, yellow dots, and short vellus hairs. In androgenetic alopecia (AGA), hair diameter diversity (HDD), perifollicular pigmentation/peripilar sign, and yellow dots are trichoscopically observed. In all cases of AGA and female AGA, HDD, more than 20%, which corresponds to vellus transformation, can be seen. In cicatricial alopecia (CA), the loss of orifices, a hallmark of CA, and the associated changes including perifollicular erythema or scale and hair tufting were observed. Different hair shafts variation such as vellus, terminal, micro-exclamation mark type, monilethrix, Netherton type, and pili annulati hairs can be seen . The number of hairs in one pilosebaceous unit can be assessed. Healthy Hair follicles variation healthy, empty, fibrotic ("white dots"), filled with hyperkeratotic plugs ("yellow dots"), or containing dead hair ("black dots"). Abnormalities of scalp skin color or structure include honeycomb-type hyperpigmentation, perifollicular discoloration (hyperpigmentation), and scaling are also seen with the help of trichoscopy.
Trichotillomania (trik-o-til-o-MAY-nee-uh), also called hair-pulling disorder, is a mental disorder that involves recurrent, irresistible urges to pull out hair from your scalp, eyebrows or other areas of your body, despite trying to stop.
Hair pulling from the scalp often leaves patchy bald spots, which causes significant distress and can interfere with social or work functioning. People with trichotillomania may go to great lengths to disguise the loss of hair.
For some people, trichotillomania may be mild and generally manageable. For others, the compulsive urge to pull hair is overwhelming. Some treatment options have helped many people reduce their hair pulling or stop entirely.Symptoms
Signs and symptoms of trichotillomania often include:
Repeatedly pulling your hair out, typically from your scalp, eyebrows or eyelashes, but sometimes from other body areas, and sites may vary over time
An increasing sense of tension before pulling, or when you try to resist pulling
A sense of pleasure or relief after the hair is pulled
Noticeable hair loss, such as shortened hair or thinned or bald areas on the scalp or other areas of your body, including sparse or missing eyelashes or eyebrows
Preference for specific types of hair, rituals that accompany hair pulling or patterns of hair pulling
Biting, chewing or eating pulled-out hair
Playing with pulled-out hair or rubbing it across your lips or face
Repeatedly trying to stop pulling out your hair or trying to do it less often without success
Significant distress or problems at work, school or in social situations related to pulling out your hair
Many people who have trichotillomania also pick their skin, bite their nails or chew their lips. Sometimes pulling hairs from pets or dolls or from materials, such as clothes or blankets, may be a sign. Most people with trichotillomania pull hair in private and generally try to hide the disorder from others.
For people with trichotillomania, hair pulling can be:
Focused. Some people pull their hair intentionally to relieve tension or distress — for example, pulling hair out to get relief from the overwhelming urge to pull hair. Some people may develop elaborate rituals for pulling hair, such as finding just the right hair or biting pulled hairs.
Automatic. Some people pull their hair without even realizing they're doing it, such as when they're bored, reading or watching TV.
The same person may do both focused and automatic hair pulling, depending on the situation and mood. Certain positions or rituals may trigger hair pulling, such as resting your head on your hand or brushing your hair.
Trichotillomania can be related to emotions:
Negative emotions. For many people with trichotillomania, hair pulling is a way of dealing with negative or uncomfortable feelings, such as stress, anxiety, tension, boredom, loneliness, fatigue or frustration.
Positive feelings.
Alopecia Areata, Dermatology Block 5.5
College of Medicine, King Faisal University, AL Ahsa, Saudi Arabia.
Alopecia Areata is A localized loss of hair in round or oval areas with no apparent inflammation of the skin
Prognosis: good for limited involvement. Poor for extensive hair loss.
Management: intralesional triamcinolone effective for limited number of lesions
Hair diseases are disorders primarily associated with the follicles of the hair. Many hair diseases can be associated with distinct underlying disorders. Hair disease may refer to excessive shedding or baldness (or both). Balding can be localized or diffuse, scarring or non-scarring.
Approach to a case of diffuse hair loss in females
. Anagen effluvium-
(a)Dystrophic
(b)Loose anagen hair
2. Telogen effluvium –
(a)acute telogen effluvium
(b)Chronic telogen effluvium
3. Female pattern hair loss
Primary CTE –represents a primary disorder and is a diagnosis of exclusion.
Secondary CTE- secondary to variety of systemic disorders.
Iron deficiency
Other deficiency –protein calorie malnutrition ,zinc deficiency
Thyroid diseases
Metabolic diseases-chronic liver or renal failure, advanced malignancy, pancreatic disease and upper GI disorder with malabsorption
SLE and other connective tissue disorders.
HIV infection
Drug induced
• In recent years, the usefulness of trichoscopy (scalp dermoscopy) (videodermatoscopy) has been reported for diagnosing hair loss diseases. This method allows viewing of the hair and scalp at X20 to X160 magnifications. Characteristic trichoscopy features of alopecia areata are black dots, tapering hairs (exclamation mark hairs), broken hairs, yellow dots, and short vellus hairs. In androgenetic alopecia (AGA), hair diameter diversity (HDD), perifollicular pigmentation/peripilar sign, and yellow dots are trichoscopically observed. In all cases of AGA and female AGA, HDD, more than 20%, which corresponds to vellus transformation, can be seen. In cicatricial alopecia (CA), the loss of orifices, a hallmark of CA, and the associated changes including perifollicular erythema or scale and hair tufting were observed. Different hair shafts variation such as vellus, terminal, micro-exclamation mark type, monilethrix, Netherton type, and pili annulati hairs can be seen . The number of hairs in one pilosebaceous unit can be assessed. Healthy Hair follicles variation healthy, empty, fibrotic ("white dots"), filled with hyperkeratotic plugs ("yellow dots"), or containing dead hair ("black dots"). Abnormalities of scalp skin color or structure include honeycomb-type hyperpigmentation, perifollicular discoloration (hyperpigmentation), and scaling are also seen with the help of trichoscopy.
Trichotillomania (trik-o-til-o-MAY-nee-uh), also called hair-pulling disorder, is a mental disorder that involves recurrent, irresistible urges to pull out hair from your scalp, eyebrows or other areas of your body, despite trying to stop.
Hair pulling from the scalp often leaves patchy bald spots, which causes significant distress and can interfere with social or work functioning. People with trichotillomania may go to great lengths to disguise the loss of hair.
For some people, trichotillomania may be mild and generally manageable. For others, the compulsive urge to pull hair is overwhelming. Some treatment options have helped many people reduce their hair pulling or stop entirely.Symptoms
Signs and symptoms of trichotillomania often include:
Repeatedly pulling your hair out, typically from your scalp, eyebrows or eyelashes, but sometimes from other body areas, and sites may vary over time
An increasing sense of tension before pulling, or when you try to resist pulling
A sense of pleasure or relief after the hair is pulled
Noticeable hair loss, such as shortened hair or thinned or bald areas on the scalp or other areas of your body, including sparse or missing eyelashes or eyebrows
Preference for specific types of hair, rituals that accompany hair pulling or patterns of hair pulling
Biting, chewing or eating pulled-out hair
Playing with pulled-out hair or rubbing it across your lips or face
Repeatedly trying to stop pulling out your hair or trying to do it less often without success
Significant distress or problems at work, school or in social situations related to pulling out your hair
Many people who have trichotillomania also pick their skin, bite their nails or chew their lips. Sometimes pulling hairs from pets or dolls or from materials, such as clothes or blankets, may be a sign. Most people with trichotillomania pull hair in private and generally try to hide the disorder from others.
For people with trichotillomania, hair pulling can be:
Focused. Some people pull their hair intentionally to relieve tension or distress — for example, pulling hair out to get relief from the overwhelming urge to pull hair. Some people may develop elaborate rituals for pulling hair, such as finding just the right hair or biting pulled hairs.
Automatic. Some people pull their hair without even realizing they're doing it, such as when they're bored, reading or watching TV.
The same person may do both focused and automatic hair pulling, depending on the situation and mood. Certain positions or rituals may trigger hair pulling, such as resting your head on your hand or brushing your hair.
Trichotillomania can be related to emotions:
Negative emotions. For many people with trichotillomania, hair pulling is a way of dealing with negative or uncomfortable feelings, such as stress, anxiety, tension, boredom, loneliness, fatigue or frustration.
Positive feelings.
Alopecia Areata, Dermatology Block 5.5
College of Medicine, King Faisal University, AL Ahsa, Saudi Arabia.
Alopecia Areata is A localized loss of hair in round or oval areas with no apparent inflammation of the skin
Prognosis: good for limited involvement. Poor for extensive hair loss.
Management: intralesional triamcinolone effective for limited number of lesions
Hair diseases are disorders primarily associated with the follicles of the hair. Many hair diseases can be associated with distinct underlying disorders. Hair disease may refer to excessive shedding or baldness (or both). Balding can be localized or diffuse, scarring or non-scarring.
Approach to a case of diffuse hair loss in females
. Anagen effluvium-
(a)Dystrophic
(b)Loose anagen hair
2. Telogen effluvium –
(a)acute telogen effluvium
(b)Chronic telogen effluvium
3. Female pattern hair loss
Primary CTE –represents a primary disorder and is a diagnosis of exclusion.
Secondary CTE- secondary to variety of systemic disorders.
Iron deficiency
Other deficiency –protein calorie malnutrition ,zinc deficiency
Thyroid diseases
Metabolic diseases-chronic liver or renal failure, advanced malignancy, pancreatic disease and upper GI disorder with malabsorption
SLE and other connective tissue disorders.
HIV infection
Drug induced
This ppt gives information about the hair structure, function of hair, hair cycle(all phase are explain in this ppt) how to maintain healthy hair during all the phase of the hair cycle.
Hair loss (alopecia) can affect just your scalp or your entire body, and it can be temporary or permanent. It can be the result of heredity, hormonal changes, medical conditions or a normal part of aging. Anyone can lose hair on their head, but it's more common in men
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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Cardiac conduction defects can occur due to various causes.
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
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4. Hair is a cutaneous appendage originally
evolved in mammals as a protective coat.
It is simple in structure, but has important
functions in social functioning
4
8. Adamson’s Fringe
Upper part of the bulb.
Keratogenous zone.
Divided into 6 layers:
1. Medulla
2. Cortex
3. Hair cuticle
4. Cuticle of inner sheath
5. Huxley’s layer
6. Henle’s layer
8
9. Follicular Papilla
Varies according to the phase of hair cycle.
Composed - specialized fibroblast like cells
embedded in extracellular matrix.
Contains a loop of capillary blood vessels.
Volume of dermal papilla maybe responsible for
controlling size of hair follicle.
9
10. Hair Shaft
3 layers :
Medulla
Cortex
Hair Cuticle
Medulla
1. Maybe continuous, interrupted or absent.
2. Contains few layers of rounded cells containing
glycogen.
10
11. Cortex
1. Forms bulk of the hair shaft.
2. Consists of numerous layers of flattened elongated
cells packed together.
Hair Cuticle
1. Consists of 5 – 10 layers of flattened cells arranged in
overlapping “roof – tile” pattern.
2. The upwards pointing edges of the hair cuticle
interlock with the downwards pointing edges of
cuticle of inner sheath.
11
12. Inner Root Sheath
1. 3 layers :
Cuticle
Huxley’s layer
Henle’s layer
2. At the Isthmus the IRS disintegrates
Outer Root Sheath
1. Most peripheral part of hair follicle.
2. Keratinize at the level of Isthmus.
3. Occasionally “companion layer” maybe seen in
between IRS and ORS.
12
14. Ultra structure of Hair
Hard keratin with high
sulfur content.
High sulfur content -
extraordinary tensile strength.
S-H linkages of cysteine at
the bulb are converted to
S-S linkages of cysteine
higher up.
14
15. Functions of Hair
Tactile perception
Protection of scalp from sunlight and trauma.
Protection of eyes from foreign bodies, sunlight &
sweat
Screening nasal passages.
Reduce friction in intertriginous areas.
Disseminates apocrine odor
Contributes to psychological perception of beauty &
attractiveness.
15
19. 19
Anagen
• Period of active hair growth.
• Duration of this phase resp. for
final length of the hair.
• Usually lasts for 2 – 6 years.
• Duration of Anagen genetically
determined.
• About 85% of all hairs are in
this phase at any time.
• Onset of mitotic activity of
epithelial cells in Dermal
papilla.
20. Lower part of follicle elongates downwards along
a preformed dermal tract ( stele ).
Dermal papilla expands .
A network of capillary blood vessels develop
around the lengthening follicle.
Epithelial cells in the hair bulb undergo vigorous
proliferative activity.
20
21. The melanocytes become active adding colour
to this newly forming hair.
Anagen consists of 6 substages.
Differences in the length of hair is due to
variable duration of the last stage ( VI ).
21
22. 22
Catagen
• Short transition stage that
occurs at the end of the
anagen phase.
• Signals the end of active
growth of hair.
• Usually lasts about 2 – 3 weeks.
• At the end of Anagen, epithelial
division declines and ceases.
• Proximal end of the hair shaft
keratinizes to form a club
shaped structure.
23. Lower part of the follicle involutes by
apoptosis.
Basement membrane surrounding the follicle
becomes thickened to form “glassy membrane”.
Base of the follicle along with dermal papilla
moves upwards to lie below the level of
Arrector muscle attachment.
23
24. 24
Telogen
• Resting phase of the hair
follicle.
• Usually lasts for about 3
months.
• About 10 – 15% of all hairs
are in this phase at any time.
• Quiscient period between
completion of follicular
regression and onset of next
anagen phase.
• Resting club hair lies within
an epithelial sac.
25. Types of HAIR
Lanugo (wool like)
Fine, soft, unmedullated, unpigmented
Vellus Hair ( ≤0.03 mm )
Soft, unmedullated, pigmented
Terminal Hair ( ≥0.06 mm )
Coarse, medullated, pigmented
25
26. Modulators of Hair Follicle Cycling in Humans
MODULATOR ACTION
Endogeneous
Androgens Promote miniaturization of follicles & shorten
duration of the anagen stage in androgen
sensitive areas of scalp;
Enlarge follicles in androgen- dependent areas
during adolescent
Estrogens Prolong anagen stage;
Post partum reduction in estrogen- telogen
effluvium
Growth hormone Acts synergistically with androgen in
adolescence
Prolactin Can induce hirsutism
Thyroxine Low levels can cause telogen effluvim;
High levels may have similar effect 26
27. Exogeneous
Anabolic Steroids Accelerate androgenetic alopecia :
Aggravate hirsutism
β Adrenergic
antagonist
Causes telogen effluvium
Cyclosporin Hypertrichosis
Estrogen Prolong duration of anagen stage
Finasteride Blocks 5 α Reductase type II
Minoxidil Induces and prolongs anagen stage & Vellus
terminal hair
OCP Cessation may cause telogen effluvium
Phenytoin Hypertrichosis
Retinoids Premature onset of catagen stage
27
28. Rate of Hair Growth :
Part of the Body Rate of Growth
Scalp 0.45mm/day
Beard 0.35mm/day
Extremities 0.25mm/day
Forehead(vellus hair) 0.03mm/day
28
29. Role of Growth Factors & Cytokines in Hair Follicle
Development,Hair growth & Hair Cycle Activity
EGF 1. Delays follicular development
2. Retards hair growth & cycling
3. Induces follicle regression & catagen–like changes in vitro
4. Stimulates elongation of hair.
TGFα 1. Controls normal positional development of hair follicle
2. Retards hair growth in vitro in mice
aFGF &
bFGF
1. Responsible for formation & maintenance of perifollicular
blood vessel
2. Important for skin appendage morphogenesis & their
formation
FGF4 1. Necessary for follicular development & epithelial
regeneration.
FGF5 1. Hair elongation inhibitor
2. Initiates transition from anagen to catagen phase 29
30. VEGF 1. Responsible for maintenance of the
perifollicular capillaries in anagen
TGFβ -1,2,3 1. Inhibits follicular development
2. Gene over expression in epidermis marked
reduction of epidermal & follicular proliferation
& dec. number of follicles in mice
BMP-2, BMP-4 1. Necessary for epithelial regeneration
NBFβ 1. Probably trophic functions for neurons
2. Probably responsible for maintenance of
perifollicular nerves in anagen
TNFα 1. Responsible for induction of apoptosis
PDGF-A,B 1. Important in follicular development &
vasculogenesis
2. Stimulates hair canal development 30
32. Alopecia is defined as “ absence or loss of hair”.
It’s a chronic disorder secondary to the disease of
either the hair follicle, hair shaft or the scalp.
32
33. Pseudoalopecia is defined as acute or chronic breakage
of hair due to congenital or acquired hair shaft
abnormalities secondary to trauma or chemicals.
Its characterized clinically by unintended short hair.
33
34. Noncicatricial Alopecia
Physiological Alopecia of infants, post-partum alopecia
Alopecia areata
Telogen effluvium
Infections Dermatophytosis, bacterial & spirochaetal infections
Chemicals & drugs: Thallium/Heparin/cancer chemotherapy/
hypervitaminosis A
Physical trauma
(self induced)
Trichotillomania, scratching of neurodermatitis
Endocrinopathy Hypo/ hyperthyroid, hypo/hyperparathyroid
Physical agents Mild trauma, epilating dose of radiotherapy, short term
hair traction
Systemic agents SLE, dermatomyositis, sarcoidosis, Langerhan’s cell
histocytosis, amylodosis 34
35. Cicatricial Alopecia
Physical trauma Long term traction of hair, x-ray
overdose burn
Infections Bacterial
Dermatophytosis
Viral
Chemical injury Caustics
Cutaneous diseases DLE, FLP,pseudopelade
Destructive neoplasms &
granulomas
Psychogenic conditions Neurotic excoriating tactile
injury to skin
35
42. Alopecia Areata
Syn. Pelade, Area Celsi
Chronic inflammatory dermatologic disorder
characterized by patchy loss of hair without
atrophy
Described by Cornelius Celsus (AD 14-37)
Term was coined by Sauvages in 1760
42
44. Genetic factors
1. MHC class I antigen HLA-DR4, DR 11 & DQ-3
2. DR4 & DR5 – ass. with severe type of AA.
3. TNF alpha has inhibitory effect on hair growth.
4. Chromosome 21
5. Atopy – early age onset & severe AA
Autoimmunity
1. Ass. – thyroid disease, anemia, DM, vitiligo, psoriasis.
44
45. Clinical Features
Smooth, localised, well demarcated patches
Progress circumferentially
Single / multiple
Scalp (90%), other regions also involved
Hairs are short, easily extractable broken ones,
called “exclamation mark” seen at margins
1 – 5 % of AA AT – 2 yrs
45
46. White hair- relatively spared, hence patients with
canitis, the onset of sudden diffuse A.A may result in hair
‘ going white’ over night.(canites subita)
Shuster described Coudability hairs ( a kink in the
normal looking hairs, 5-10mm above the surface ,when
the hair is bent inwards).
46
55. Poor prognosis
Atopy
Other immune disease
Family H/o AA
Excessive hair loss
Oophiasis pattern
Nail dystrophy
Poor patient compliance
55
56. Investigations
Hair – Pull test
Hair pluck test
Dermoscopy
SALT score ( severity of alopecia tool score)
Optical Coherence Tomography- detect hair
shaft abnormalities.
56
57. Histopathology
Peribulbar and intrabulbar inflammatory infiltrate
concentrated in and around hair bulb giving “swarm
of bees” appearance.
Infiltrate mostly of T lymphocytes and macrophages
present around the matrix and dermal papilla.
Miniaturization of hair follicles.
57
62. CS’s
1. Hydrocortisone acetate 25mg/mL
2. Triamcinalone acetonide 5-10mg/mL
3. Accelerates regrowth
4. SE- Atrophy,pain,tingling - reversible
Anthralin
1. .25%-.1% used
2. SE-irritation, scaling, folliculitis, stains
3. 1st line Rx in children
4. Growth occurs in 3mths
5. Total application time 6mths
62
63. Alopecia totalis treated with topical immunotherapy (2,3-
diphenylcyclopropenone): (A) before treatment; (B) unilateral
hair regrowth after 15 weeks of unilateral treatment; (C)
complete regrowth after 42 subsequent weeks of bilateral
treatment. Courtesy of R Happle, University of Marburg, Marburg, Germany63
64. Telogen Effluvium
The term Telogen effluvium –first coined by Kligman.
Telogen hair- resting hairs with non pigmented club tip at
the proximal root & easily plucked from the scalp.
In this cond. premature covertion of anagen hair to
telogen hair takes place resulting in disproportionate
shedding & dec. in the total number of hair.
64
65. Etiology
Physiologic
1. Physiologic effluvium of new born
2. Postpartum effluvium
3. Early changes of androgenic alopecia
4. Injury/ stress
5. High or prolonged fever
6. Severe infection
7. Severe chronic illness
8. Severe psychologic stress
9. Major sugery
10. Hypothyroidism & other endocrinopathies
11. Severe dieting or malnutrition
65
67. Diagnosis
Detailed patient history (drug/diet)
Complete blood count
TFT
Hair –pull test
Trichogram
ANA titre
Sr. Zinc levels
VDRL
67
68. Treatment
Normal hair growth occurs with time & resolution of
underlying causes.
No specific treatment – required
In case of no recovery – minoxidil can provide some
benifits
68
69. Androgenetic Alopecia
Androgenic alopecia is hereditary thinning of the hair
caused due to androgens in genetically susceptible men
& women.
In males, male pattern hair loss / common baldness.
In females, female pattern hair loss.
69
70. Clinical features
MPHL- easily recognized
1. Described – Hamilton & Norwood
2. Thinning of hair in frontal & vertex area with
progression of hair loss
3. Marginal parietal & occipital hair – retained.
70
72. FPHL- differ from men.
1) Described by Ludwig
2) Diffuse thinning over the crown with no H/O
shedding.
3) In women, hair thinning begins – frontal & later
involve the entire scalp sparing the frontal hairline.
4) Hair density remains the same, hair no longer grows
into its previous length.
72
74. Hair Loss Severity Classification
For MPHL, Norwood/ Hamilton scale
For FPHL, Ludwig’s classification scale
74
75. Pathology
l
Marked reduction in terminal hairs
Miniaturization of hair follicles increase in secondary
vellus hairs
Mild perifollicular infiltrate mostly lymphohistiocytic
with or without concentric layers of perifollicular
collagen deposition
75
79. Evaluation of Hair loss
History & Examination
1. Time period of hair loss(congenital, acquired)
2. Progression of hair loss
3. Any positive family history
4. H/o G.I dysfunction, thyroid gland dysfunction
, psychological disorders
5. H/o any surgical intervention / chronic illness
6. All medications
7. In females, menstrual & obstetric history
8. Hair care routine/ hair products
79
81. Disease Common pattern seen
Diseases with patterned loss
Androgenic alopecia Women – central thinning
Men -- ‘M’ shaped thinning
Syphilis ‘Moth eaten ‘ appearence
Trichotillomania Bizarre, incomplete thinning ,stubble
Diseases with diffuse hair loss
Alopecia universalis Body & scalp involved
Telogen effluvium alopecia totalis , chemotherapy
or drug induced metabolic disorders
Diseases with focal loss
Alopecia areata Patchy hair loss
Tinea capitis Fragile & easily broken hair
Trichotillomania Patchy, incomplete thinning with
stubble
Traction alopecia Frontal & temporal loss of hair
Cicatricial alopecia Presence of cellulitis or folliculitis81
82. Blood Investigations
Complete blood count
VDRL
Sr. iron
Sr. ferritin
Total iron binding capacity
TFT
Antinuclear factor –DLE
Hormone levels
82
84. Scalp Scores
Global photographs
Head shots taken at a short distance away from the
patient who is seated in front of a plain cloth.
Standard global views- vertex, midline, frontal, temporal.
GB’s – taken before and at various stages of treatment
Rating – 7 point scale (-3 to +3)
84
86. Macrophotographs – 4 times magnification
_ density & diameter of hair
Area 14mm x 13mm
Density graded 1 to 6
1- fewer than 4 hairs
6- more than 40 hairs
Diameter graded 1 -thin
2 -medium
3 -thick
86
87. Regional Hair pattern
The pattern of hair loss in androgenic alopecia is
well defined & distinct in both men and women.
Norwood – Hamilton scale - male
Ludwig scale - female
87
90. Contrasting Felt Examination
AIM- To see the short, miniature hairs of the scalp.
PROCEDURE- An index card with black felt glued
on one side and white felt on the opposite side is
used.
After parting in the hair, the index card is held
along the scalp
90
91. INFERENCE- Fine short
hairs with broken or tapered
distal tips project up along
the edge of the felt.
These miniature hairs –
in the androgen dependent
areas both men & women.
91
92. Daily Hair Counts
Useful for quantitative assessment of the actual number of
hairs shed daily in patients with complaints of excessive
shedding.
Collect for 14 consecutive days
Average daily loss – 30-70 hairs /day.
If >70 hairs – microscopic examination is done to
detect pathology.
92
94. Semi-invasive methods
Hair Pull Test
Hair Feathering Test
Trichogram( Hair Pluck Test)
Unit Area Trichogram
Phototrichogram & Videotrichogram
Digital Epiluminescence Microscopy
Global Photographs in Phototrichogram
94
96. Telogen hair is easily extracted than anagen hair
PROCEDURE-
1. About 60 hairs- pulled with constant traction
2. Bulb of extracted hair is examined
3. The number of telogen hair is counted
4. Expressed as percentage of total hair pulled
Upto 7% - normal
>10% - effluvium
Telogen effluvium, anagen effluvium, loose anagen syndrome,
early cases of patterned alopecia and the advancing edge of
alopecia areata
96
97. Other drawbacks of this test:
Washing hair before- may give false low No. of telogen hair.
Frequency of telogen shedding varies day to day.
Seasonal variation – inc. spring & autumn.
More in the frontal & vertex region compared to occipital
region.
Alopecia - failure of development of new anagen hair rather
than increased telogen hair ratio. In these patients hair pull
test is normal.
97
98. Hair Feathering Test
AIM- detecting abnormal hair fragility and hair shaft
breakage.
PROCEDURE-
1. Distal 2 to 3cm – hairs in involved areas – grasped &
pulled.
2. Grasped hair - checked for broken fragments
3. Microscopic examination- confirms nature of hair
shaft defect & type of fracture.
98
100. The plucked hairs are arranged side by side
on a glass slide and taped
100
101. Anagen hair - forcibly
plucked terminal anagen
hair showing the pigmented
bulb with 'hockey-stick'
appearance.
101
102. Telogen hair - forcibly plucked
early telogen hair showing the
hypopigmented, club-shaped
cornified bulb
with remanents of the cornified
epithelial sac.
102
103. Unit Area Trichogram
In a marked out area (30mm2) – hair is epilated- the
proportion of various type of hair is counted.
A/T ratio, shaft diameter, density.
Av. diameter – healthy hair- ≥ 80μ𝑚.
103
104. Phototrichogram
Phototrichogram was introduced by Saitoh in
1970
Technique that allows in vivo study of physiology
of the hair cycle and measurement of various hair
growth variables.
104
105. These variables are:
1. Hair density
2. Hair thickness
3. Hair length
4. Linear growth rate.
105
106. PROCEDURE-
Day 0 t(0) -Clipping the hair short (1mm) in a marked
area.
Photograph is taken- high magnification
Day 2 (t2)
After 48 h, the second photograph was taken
Patient advised – not to wash hair
106
107. INFERENCE-
1. Hair variables at Day 0
Density of hair in the specified area
Length of hairs (L1)
2. Hair variables at Day 2
The length of hairs (L2)
Hair growth in mm/day, (L2-L1)/2
Number of hairs showing hair growth.(Anagen hairs)
Number of hairs not grown. (Telogen hairs)
107
115. Main actions of Minoxidil on the hair follicle;
1. Inc. in the proportion of hair - anagen phase by promoting
premature entry of the hair follicle into the anagen phase
2. Prolongs the length of anagen phase
3. Dec. the no. of follicles – telogen phase
4. Inc. – hair follicle size & hair diameter
On topical application- rapid inc. of hair growth is seen as soon as
6 to 8 weeks & max. effect at 12 to 16 weeks.
115
117. Finasteride
It’s a competent & specific inhibitor – type II 5α-reductase
enzyme.
Prevents testosteroneDHT.
65% bioavaiability.
90% of circulating drug bound to plasma protein.
Crosses the BBB.
Metabolized in liver, via cytochrome P450 enzyme.
Metabolites formed in liver –excreted in faeces with 40%
in urine.
117
118. Indications & Dosage
Androgenic alopecia with mild to moderate hair loss
of vertex & ant. mid scalp area.
Its effectiveness in bitemporal recession has not been
established.
Recommended dosage- 1mg orally OD daily use ≥3
months.
Withdrawal of drug – revesal effect in 12 months.
118
119. Adverse effects
Breast tenderness & enlargement
Hypersensitivity reactions-
Pruritus, rash, urticaria , swelling of lips &
face, testicular pain.
Erectile dysfunction.
Less libido.
119
120. Contraindications
In women- child bearing group & pregnant women
In children
In patients hypersensitive to drug.
120