Disorders of the hair shaft present with a challenge while understanding the topic and also while diagnosing any patient presenting with a similar problem. This presentation makes the approach to any patient presenting with hair shaft disorders more comprehensive.
• 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.
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
• 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.
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
Pigmentation disorders of skin dermatology revision notesTONY SCARIA
dermatology revision notes for neet pg preparation based on lecture notes with high yield topic & last minute revision notes based on previous year questions
They are a heterogenous group of inherited disorders of epidermal differentiation featuring excessive scaling, Ichthyosis vulgaris,
X-linked recessive ichthyosis,
Lamellar ichthyosis,
Non-bullous ichthyosiform erythroderma,
Bullous ichthyosiform erythroderma,
Ichthyosis bullosa of Siemens,
Harlequin ichthyosis
Mucins are jelly-like acid glycosaminoglycans (formerly known as mucopolysaccharides) of the ground substances and probably play a part in the extravascular exchange of metabolites. Mucin is normally produced in small quantities by fibroblasts. Acid glycosaminoglycans, such as hyaluronic acid and heparin, stain with toluidine blue, colloidal iron, or with alcian blue at pH 2.5, the coloration depending on the number and nature of the acid groups. PAS stains heparin, but not hyaluronic acid. In general, acid glycosaminoglycans stain much brighter in frozen fixed tissue, or in 1% cetylpyridinium chloride solution, rather than in formalin-fixed biopsies.
Classification of the cutaneous mucinoses:
1- Primary
2- Secondary
Pigmentation disorders of skin dermatology revision notesTONY SCARIA
dermatology revision notes for neet pg preparation based on lecture notes with high yield topic & last minute revision notes based on previous year questions
They are a heterogenous group of inherited disorders of epidermal differentiation featuring excessive scaling, Ichthyosis vulgaris,
X-linked recessive ichthyosis,
Lamellar ichthyosis,
Non-bullous ichthyosiform erythroderma,
Bullous ichthyosiform erythroderma,
Ichthyosis bullosa of Siemens,
Harlequin ichthyosis
Mucins are jelly-like acid glycosaminoglycans (formerly known as mucopolysaccharides) of the ground substances and probably play a part in the extravascular exchange of metabolites. Mucin is normally produced in small quantities by fibroblasts. Acid glycosaminoglycans, such as hyaluronic acid and heparin, stain with toluidine blue, colloidal iron, or with alcian blue at pH 2.5, the coloration depending on the number and nature of the acid groups. PAS stains heparin, but not hyaluronic acid. In general, acid glycosaminoglycans stain much brighter in frozen fixed tissue, or in 1% cetylpyridinium chloride solution, rather than in formalin-fixed biopsies.
Classification of the cutaneous mucinoses:
1- Primary
2- Secondary
alopecia hair loss Alopecia is a disease that causes hair loss.pptxittielarathi
Alopecia is a disease that causes hair loss. Most people lose hair on their scalp or beard area, but hair loss can occur anywhere on your body. A board-certified dermatologist can tell you if you have this type of hair loss and what may help you regrow your hair.
This is my very first power point. I made it for my Human Anatomy class. There is not any special features because we only had to turn in hard copies. This was a really easy and entertaining assignment!
Progressive miniaturization of terminal hair is the hallmark of pattern hair loss. Miniaturization is a process in which large, pigmented terminal hair is replaced by fine colorless vellus hair, because of the shortening of the anagen phase in consecutive hair cycles. Pattern hair loss affects both males and females as progressive thinning of hair is a pattern that is different between males and females. Male pattern hair loss (MPHL) increases in frequency and incidence as age advances after puberty. MPHL is characterized by thinning of hair in the frontal, frontotemporal, and vertex areas of the scalp with variable loss of marginal, parietal, and occipital hair. Diagnosis is made clinically based on the history of hair thinning, hair loss, local examination, and a few simple tests. Anisotrichosis is finding on dermoscopy. The two main causative factors responsible are genetic predisposition and a derivative of testosterone, dihydrotestosterone (DHT). This is autosomal dominant and polygenic. The gene is X chromosome-linked indicating maternal component. Testosterone is converted by an enzyme 5-alpha reductase, into a more potent metabolite, Dihydrotestosterone, which is responsible for MPHL There are two types of 5- alpha-reductase, type one and type two. Finasteride is a competitive inhibitor of 5 α Reductase type II, while Dutasteride inhibits both alpha type I and type II. Finasteride and minoxidil are US-FDA approved as medical treatment of MPHL. The medical treatment is effective if started in the early phase of hair loss. . There are few side effects of finasteride, but the incidence is very low, and they are reversible once the finasteride is stopped. Medical treatment is not to treat the developed baldness. The treatment of baldness is the transplantation of hair follicles.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Case Scenario 1
• A 9 year old boy presented with unruly hair since birth. Although his
hair appeared to have normal growth without excessive loss or
increased brittleness, it did not maintain its shape after styling. His
elder sister had experienced similar hair problems during childhood
but the condition had disappeared spontaneously with puberty. The
hair of the other immediate family members was normal.
6. Complaints:
• My hair doesn’t grow long/ never had a haircut
• Unusual appearance /texture
• Suddenly started breaking
• Complete cessation of hair growth
• When did the problem first start?
• Are there any problems with nails or teeth
• How does the patient dress/style the hair? Brushing technique,
frequency of shampooing, use of heat and chemicals.
7.
8.
9. HAIR CARD TEST
• 8 * 12 cm piece of paper
• White on one side and black on
other side.
• Place the card on the scalp and
against the hair shafts in the
affected area.
• Broken hairs or regrowing hairs??
10. HAIR PULL TEST:
• Affected area- (50-60) hairs
• Pull along the hair shafts
• 4 different regions
• prerequisite?
• More than 5/6 hairs pulled out(10%)?
12. HAIR MOUNT:
• Asses hair bulb and shafts using light microscopy.
• HAIR BULBS: epilated hair roots placed on a glass slide . Add a
mounting medium. Add cover slip
• Anagen vs Telogen?
• HAIR SHAFT: bubbles, irregularities, twisting,fractures
13. TRICHOSCOPY:
• Magnified observation of: hair shafts, hair follicle openings,
perifollicular epidermis , blood vessels.
• Normal terminal hair: uniform thickness, color throughout the
length.
• Vellus hairs: lightly pigmented, measure < 3 mm in length and < 30
microns in thickness.
• Regrowing hairs: darkly pigmented, straight with pointed ends
14.
15.
16.
17. IS THERE HAIR BREAKAGE?
(FRAGILITY)
YES NO
PRESENT SINCE BIRTH?
CONGENITAL CONGENITALACQUIRED
• MONILETHRIX
• PILI TORTI
• TRICHORRHEXIS
NODOSA
• TRICHOTHIODYSTROPHY
• TRICHORRHEXIS
INVAGINATA
• BUBBLE HAIR
• ACQUIRED
TRICHORRHEXIS
NODOSA
• TRICHOPTILOSIS
• PILI ANNULATI
• PSEUDOPILI ANNULATI
• WOOLLY HAIR
• UNCOMBABLE HAIR
SYNDROME
• PILI BIFURCATI
• PILI MULTIGEMINI
• LOOSE ANAGEN HAIR
SYNDROME
• SHORT ANAGEN HAIR
SYNDROME
18. ACQUIRED HAIR SHAFT DISORDERS WITH
INCREASED FRAGILITY AND BREAKAGE
• BUBBLE HAIR:
1. Bubbles within hair cortex
2. High temperature :blow dryers/curling irons
3. Unruly and ‘fly-away’ hair
4. Excess lint and hair blocking intake of air into dryer.
5. 17.5 deg Celsius to 21.5 deg Celsius for 5 minutes
6. Damp hair.
7. Cuticular defects and focal loss of cortical cells and medulla at sites
of bubbles.
21. TRICHORRHEXIS NODOSA
• Hair shaft fractures.
• Chemical, thermal, mechanical damage to hair shaft
• Acquired type: proximal and distal
• Change in quality of hair/dry hair/hair that won’t grow.
• Nodes at different sites along different hair shafts.
• Loss of shine
• malnutrition/metabolic disorders
• Association: pili annulati
22.
23. • Trichoscopy:
• Light colored nodules or gaps along hair shaft
• Fractured ends= brush like appearence
24.
25. TRCHOPTILOSIS:
• Split ends.
• Longitudinal splitting –distal end of hair
• Short hairs-friction /trichotillomania
• Trichoscopy: longitudinal splitting of the distal hair shafts. 2 or more
frayed ends of different length.
26. CONGENITAL HAIR SHAFT DISORDERS WITHOUT
INCREASED FRAGILITY
1. UNCOMBABLE HAIR SYNDROME(spun glass hair, cheveux
incoiffables, pili trianguli et canaliculi):
• unruly hair, difficult to style, standing away from the scalp
• Childhood, acquired also reported.
• Ocular, dental, ectodermal defects.
• Improves with ageing
• SEM: gold standard.
• HAIR MOUNT: canal-like longitudinal groove along one or two facets
• Examination of hair cross sections/Trichoscopy: triangular or kidney-
shaped appearance of hair shaft.
27.
28.
29. 2.PILI ANNULATI (Ringed hair):
• Non-fragile
• Glittery or spangled appearance
• Bright and dark bands.
• Scalp, axilla, beard, pubic areas
• BRIGHT BANDS= abnormal air filled cavities within cortex.
• HAIR MOUNT: bright bands appear dark
• Autosomal dominant
• 12q
• Association: alopecia areata, trichorrhexis nodosa
30.
31. • TRICHOSCOPY:
• Alternating white bands corresponding to air-filled cavities.
• Confusion with: intermittent medulla of thick hair shafts.
(light-colored, less than 50 % of shaft width)
32.
33. CASE SCENARIO:
• A 5-year-old girl child presented with abnormal patch of hair since 2 years of age.
Her parents noticed a single patch of curling and coiling of hair along with altered
texture over the left side of scalp. Her parents felt the patch to be unruly and
unsightly and hence attempted repeated tonsuring. In spite of this, the patch of
hair remained the same.
• Birth and development history of the child was normal.
• Her family members did not have similar complaints.
34. Examination:
• solitary circumscribed patch of size 6×4 cm
• left frontoparietal region of scalp.
• hair over the patch had an altered texture, was lighter in color, thinner, tightly
coiled, and curled giving an unkempt appearance.
• The skin over the patch was apparently normal.
• Examination of rest of the scalp, teeth and nails were also normal.
• There was no evidence of palmoplantar keratoderma and evidence of any
epidermal nevus elsewhere.
• Ophthalmic and cardiac evaluation did not reveal any abnormality.
38. HEREDITARY WOLLY HAIR FAMILIAL WOLLY HAIR
AD AR
NOT ASSOCIATED WITH
HYPOTRICHOSIS
HYPOTRICHOSIS +
VARIABLE HAIR COLOR SPARSE ,THIN ,SHORT
A/W-CARVAJAL/NAXOS LPAR6, LIPH GENE
39. • DERMATOSCOPY:
• Hair shafts resembling a crawling snake with short wave cycles.
• Broken hair shafts which correspond to increased fragility of hair shafts
due to longitudinal twisting.
40.
41. Woolly hair nevus:
• Discrete area of tightly curled hair.
• Otherwise normal scalp.
• Sporadic.
• Normal growth/slower growth.
• Birth/ before 18 months of age.
• 50% associated with linear naevi.
• Epidermal naevi: neck, arms or trunk
• Neurological defects, ocular abnormalities, bone disorders and
mesodermal defects.
42. PILI BIFURCATI AND PILI MULTIGEMINI:
• Hair shafts from same papilla.
• Irregular configuration,longitudinal grooving, areas of bifurcation and
re-adhesion of shafts.
• PILI BIFURCATI: protein deficiency and mosaic trisomy 8 syndrome.
• PILI MULTIGEMINI: cleidocranial dysostosis, trichorhinophalangeal
syndrome.
• Along jaw lines.
43. LOOSE ANAGEN HAIR SYNDROME:
• Anagen hairs- loosely anchored and easily pulled from scalp.
• Fair-haired, girls , 2-9 years
• Unruly, uneven, patchy, never needs a ‘cut’.
• Stiff uncombable hair/excessive shedding of hair.
• Hair pull test: positive
• HAIR MOUNT: ruffling of cuticle adjacent to anagen bulb, ‘floppy sock
appearance’, twists and grooves .
• Associations: ectodermal dysplasia, coloboma,EB,Noonan syndrome
44. Diagnostic criteria:
• Tosti et al:
1. Positive pull test with painless extraction of atleast 10 LAH
2. Presence of atleast 80% LAH on trichogram, revised to 70%.
45.
46. CONGENITAL HAIR SHAFT DISORDERS WITH INCREASED
FRAGILITY AND BREAKAGE:
• MONILETHRIX
• PILI TORTI
• TRICHORRHEXIS NODOSA
• TRICHOTHIODYSTROPHY
• TRICHORRHEXIS INVAGINATA
48. CASE SCENARIO:
• 5-year-old boy presents with his mother, who reports that whenever he has a fever
and has to lie in bed for a few days, his hair breaks off from friction of his head lying
on the pillow. Following a recent febrile episode, he comes in with short, uneven,
broken hair. His mother also reports that he has always had dry skin and ‘‘does not
do well’’ in the sun. The patient’s medical history includes mild mental and
developmental impairment. A tug test is positive, indicating hair fragility. With
polarizing microscopy the hair has a banded or ‘‘tiger tail’’ appearance . The hair is
sent for amino acid analysis.
49.
50. TRICHOTHIODYSTROPHY
• AR
• 3 different gene mutations: XPD,XPB,TTDA
• Cystine deficient brittle hair.
• Phenotypes: brittle hair only to neuroectodermal symptom complex.
• Short, fragile hair
• Photosensitivity, ichthyosis, intellectual impairment, decreased fertility, short
stature, immunodeficiency.
• HAIR MOUNT: undulating ,wavy outline, trichoschisis fractures, TN like
fractures, ribboning
• POLARIZING MICROSCOPY: alternating bright and dark( tiger tail) bands.
• AMINO ACID ANALYSIS: reduced cystine content to less than half of normal.
51. DERMATOSCOPY:
• Tiger tail pattern not visible on dermatoscopy
• Non-homogenous structure of “grains and sand” and slightly wavy
contour.
52.
53. PILI TORTI:
• Spangled appearance due to unequal reflection of light from twisted
surface.
• Patchy hair breakage and coarse stubble –occiput ,temporal areas
• Eyebrows and eyelashes involved
• Isoated.
• Asscoated with: neurological/ectodermal disorders
• why? Irregularity in IRS/ Reactive oxygen species secondary to
mitochondrial dysfunction.
• LIGHT MICROSCOPY: flattened hair twisted at 180 degrees along its axis at
irregular intervals and in groups of (3-10). Without mounting media
54.
55. PILI TORTI:
• Acquired: retinoids, anorexia nervosa
• DERMATOSCOPY: Hair shafts with sharp bending at irregular
intervals.
56.
57. Bjornstad syndrome:
• AR
• Pili torti + b/l congenital SNHL.
• Before 2nd yar of life
• Severity of hair involvement directly correlates with degree of hearing
loss.
• BCSIL gene mutation
• Pili torti improves with age.
61. TRICHORRHEXIS INVAGINATA:
• NETHERTON SYNDROME: trichorrhexis invaginata + ichthyosis linearis
circumflexa +atopic diathesis
• Erythroderma, FTT
• Eczema like eruptions,AD,asthma, allergic rhinitis,angioedema
,urticaria
• HAIR: eyebrow/limb hair- bamboo hair
• HAIR MOUNT: intussusceptions resembling ball and cup joints of
bamboo joints . Cup portion= proximal, ball portion=distal
62.
63. TRICHOSCOPY:
• Hair breakage with ball shaped nodes,invaginations and golf-tee
endings
• EYEBROWS: bamboo hairs, golf-tee hairs, matchstick hairs
64.
65.
66. CASE SCENARIO
• Two siblings aged 24 and 21 years, born of nonconsanguineous
marriage, presented with progressive, diffuse hair loss and thinning of
hair over the scalp since 14 years and 8 years, respectively. The
complaints were not associated with seasonal variation or trauma to
the hair. There was history of similar complaints in the father.
67. Examination
• sparse hair over the axillae and scalp involving the frontoparietal and
temporal areas with relative sparing of the occipital area.
• Multiple keratotic papules were noted over the nape of the neck and
the dorsal aspect of the forearms bilaterally.
• TRICHOSCOPY: hairs over the occipital region and axillae revealed hair
shafts having uniform elliptical nodes with intermittent constrictions
and bent regularly at multiple locations along with a majority of
broken hair
68.
69. MONILETHRIX (Necklace hair):
• AD
• Mutation of type 2 basic keratin hHb1 and hHb6
• AR variant – Dsg 4 mutation ,a/w localised hypotrichosis, affected hairs
have perifollicular papules caused by ingrown hairs.
• Beaded hair
• Naked eye
• Scalp mainly occipital , entire body hair can be affected.
• Keratosis pilaris on shoulder and upper back
• Koilonychia, brittle nails, syndactyly, juvenile cataracts, decreased visual
fields and dental lesions
• Improve with puberty,pregnancy,OCP
70.
71. • Severity varies within family.
• DERMATOSCOPY: hair shaft beading, elliptical nodes, regularly
separated by narrow internodes(sites of fracture)
• REGULARLY BENDED RIBBON SIGN: regular bends at multiple
locations with aa tendency to curve in different directions.
• PSEUDOMONILETHRIX: irregular intermittent constrictions,presence
of medulla, absence of ribbon sign.
• AR monilethrix: internodes are more numerous and causes severe
breakage.
72.
73.
74.
75.
76.
77. REFERENCES
1. Rakowska, Adriana, Monika Slowinska, Elzbieta Kowalska-Oledzka, and Lidia Rudnicka.
“Trichoscopy in Genetic Hair Shaft Abnormalities.” Journal of Dermatological Case Reports 2, no.
2.
2. Mubki, Thamer, Lidia Rudnicka, Malgorzata Olszewska, and Jerry Shapiro. “Evaluation and
Diagnosis of the Hair Loss Patient.” Journal of the American Academy of Dermatology 71, no. 3
(September 2014): 415.e1-415.e15.
3. Miteva, Mariya, and Antonella Tosti. “Dermatoscopy of Hair Shaft Disorders.” Journal of the
American Academy of Dermatology 68, no. 3 (March 2013): 473–81.
4. Mirmirani, Paradi, Kathie P. Huang, and Vera H. Price. “A Practical, Algorithmic Approach to
Diagnosing Hair Shaft Disorders: A Practical, Algorithmic Approach to Diagnosing Hair Shaft
Disorders.” International Journal of Dermatology 50, no. 1 (January 2011): 1–12.
5. Rook’s textbook of Dermatology,9th edition
6. Dermatology, 4th edition, Jean L. Bolognia
