Dermatology Power point slides Useful, Important & Easy Way To Understand The Chapter

1. DR. BIJAY Kr. Yadav
Holy Vision Technical Campus
Shankhmul, Kathmandu
Dermatology Department

2. Introduction
 Hair loss is often a cause of great
concern to the patient for cosmetic and
psychologic reasons.
 It can also be an important sign of
systemic disease.

3. Classification
1. Scarring alopecia permanently destroys the
hair follicle. e.g, bullous diseases,
chemical alopecia, DLE, folliculitis, lichen planopilaris,
dissecting cellulitis, and tumors
2. Nonscarring alopecia hair loss without
permanent destruction of the hair follicle. e.g, anagen
effluvium, androgenetic alopecia, chemical alopecia,
folliculitis (mild), inherited disorders of the hair shaft, telogen
effluvium, alopecia areata, and traumatic alopecia.
3. Diffuse or localized

4. Each cycle consists of a long growing phase (anagen),
a brief transitional apoptotic phase (catagen), and a
short resting phase (telogen)

5. Hair cycle

6. Normal hair cycle
 Scalp hair grows in cycles, with each hair follicle
undergoing 10 to 30 cycles in its lifetime.
 Diffuse hair shedding is the result of a disruption of
one phase of the hair cycle, ie, anagen (active hair
growth), catagen (involution), or telogen (resting)
 The anagen phase can last 2 to 8 years, the catagen
phase lasts 4 to 6 weeks, and the telogen phase lasts
2 to 3 months

7.  Most people have about 100,000 scalp hairs.
 normally 10% to 15% of these are in the telogen
phase, rest 85-90% in Anagen phase.
 Shedding of 100 to 150 telogen hairs per day is
normal.

8. Differential diagnosis of Diffuse hair loss

9. Telogen effluvium
 Is the most common cause of diffuse hair loss.
 Anagen-phase hair follicles prematurely transits
to the telogen phase,
 Results in a noticeable increase in hair shedding
at the end of the telogen phase 2 to 3 months
later.

10. Classified as
 Acute (lasting < 6 months) If a trigger is acute and
short-lived, likely be acute and will resolve.
 Chronic (6 months or more) If a trigger is ongoing,
if repeated or sequential triggers occur, or if a
trigger is not reversed, then the telogen hair
shedding can be ongoing.

11. Triggers of Telogen hair loss
 Physiologic stress
Physiologic stress such as surgical trauma, high
fever,chronic systemic illness, post-partum and
hemorrhage are well known to cause telogen
effluvium 2 to 3 months after the insult
 Emotional stress
The relationship between emotional stress and hair
loss is difficult to ascertain, and hair loss itself is
stressful to the patient

12.  Dietary triggers
Nutritional causes are zinc deficiency and iron deficiency.
Severe protein, fatty acid and caloric restriction with chronic
starvation and crash dieting.
Malabsorption syndromes and pancreatic disease .
Others are vit d def, biotin def

13. Contd....
 Medical conditions
 Both hypothyroidism and hyperthyroidism
 systemic amyloidosis,
 hepatic failure,
 chronic renal failure,
 inflammatory bowel disease,
 autoimmune diseases such as systemic lupus
erythematosus and Dermatomyositis.

14. Drugs known to cause telogen effluvium are :
 Oral contraceptive pills,Changing or stopping any oral
contraceptive can precipitate telogen hair shedding
 Androgens
 Retinoids
 Beta-blockers
 Angiotensin-converting enzyme inhibitors,
 Anticonvulsants
 Antidepressants
 Anticoagulants heparin and warfarin (Coumadin)
 Stars on 12th weeks & continues while on the drug

15. How to identify the triggers?
 The relationship between the trigger and the hair
loss must be reproducible, with improvement of the
hair shedding following correction of or removal of
the trigger, and deterioration on re-challenge.
 A detailed history is important to determine an
accurate timeline.

16. Taking the history: Identifying triggers of
diffuse hair loss
 Duration of hair shedding Episodic or continuous
hair shedding
 Estimation of percentage hair lost
 Identification of triggers and their temporal
relationship to the hair shedding
 Recent surgery, fever, illness, childbirth,
psychological stress
 History of chronic disease, malignancy, infection,
autoimmune disease, liver or renal disease

17. Contd...
 Hair care procedures
 Dietary history and weight loss noted
 Family history of androgenetic alopecia, alopecia
areata, autoimmune disease, thyroid disorder
 Medication history including over-the-counter
drugs and botanicals
 History of radiation therapy or exposure to heavy
metals

18. ANAGEN HAIR LOSS:
 Due to interruption of the anagen hair cycle, presents
as abrupt anagen hair shedding with a severe diffuse
scalp alopecia.
 The time course for anagen effluvium is usually rapid
compared with telogen effluvium, occurring within days
to weeks of the insult to the hair follicles.
 The hair-pull test is positive for dystrophic anagen
hairs with tapered ends.
 If the insult ceases, hair growth restarts again within
weeks. (reversible)

19. Etiology
 Antimitotic chemotherapeutic agents induce arrest
of the anagen phase and present a toxic insult to
the rapidly dividing hair matrix.
 Other causes are radiation, heavy-metal
poisoning, and boric acid poisoning.

20. Alopecia Areata
 Alopecia areata is sudden patchy hair loss in people with no obvious
skin disorder or systemic disease.
 Is thought to be an autoimmune disease affecting genetically
susceptible people exposed to unclear environmental triggers, such
as infection or emotional stress.
 Patches may be single or multiple, and may coalesce
 Although most obvious on the scalp, any hair-bearing skin can be
affected, and is frequently found to involve the beard area.

21.  Family history is positive in 25% of affected.
 It occasionally coexists with autoimmune vitiligo or
thyroiditis.
 Manifests as discrete circular patches of hair loss
characterized by short broken hairs at the
margins, which resemble exclamation points

23. Exclamation hair sign

24. The term alopecia totalis is used to
describe complete loss of terminal
hair on the scalp and alopecia
universalis to describe total loss of
all terminal hair on the scalp and
body

25. Prognosis
 Spontaneous remission can be expected in the
majority of cases where hair loss is limited to a few
small patches (possibly, up to approximately 80
percent within 1 year),

26. Poor prognostic factors :
 Onset in childhood
 Severe disease ( Alopecia totalis, universalis)
 Duration >1 yr
 Nail Disease
 Atopy
 Ophiasis

27. Physical examination :
 The scalp should be examined for degree and pattern of hair
loss.
 Hair shedding is increased
 Hair loss is generalized or localized
 Associated symptoms such as pruritus and scaling should
be noted
 Patients should be asked about typical hair care practices,
including use of Braids, Rollers, and Hair dryers, and
whether they routinely pull or twist their hair

28.  Full skin examination should be done to evaluate hair
loss elsewhere on the body (eg. Eyebrows, Eyelashes,
Arms, Legs)
 Associated skin diseases(eg, Lichen planus, Atopy,
Psoriasis, Discoid lupus lesions, Hidradenitis, signs of
secondary syphilis or of other bacterial or fungal
infections)
 Signs of virilization in women (eg, Hirsutism, Acne,
Deepening voice, Clitoromegaly).
 Signs of potential underlying systemic disorders should
be sought, and a thyroid examination should be done.

29. Evaluation of hair loss :
Pull test :
 Gentle traction is exerted on a bunch of hairs (40
to 60) on at least 3 different areas of the scalp,
and the number of extracted hairs is counted and
examined microscopically.
 Normally, < 3 telogen-phase hairs should come
out with each pull. If at least 3 hairs are obtained
with each pull or if > 10 hairs total are obtained,
the pull test is positive and suggestive of Telogen
effluvium

30. Pluck test (Trichogram) :
 Pulls individual hairs out abruptly (“by the
roots”). The roots of the plucked hairs are
examined microscopically diagnose a defect of
telogen or anagen or an occult systemic
disease.
 Anagen hairs have sheaths attached to their
roots & are pigmented; telogen hairs have tiny
bulbs without sheaths at their roots & non-
pigmented.

31. Investigations :
 A complete blood count and serum ferritin
level to look for anemia and iron deficiency
 A thyroid-stimulating hormone and
thyroxine (T4) level to detect thyroid disease
 A serum zinc level to detect zinc deficiency
 A comprehensive metabolic panel to
exclude chronic renal or liver disease.

32. Indications of scalp biopsy :
 Scalp biopsy is helpful in most cases of
hair loss.
 Lack of identifiable triggers, chronic hair
loss, miniaturized hair shafts, and failure to
exclude alopecia areata

33. Androgenic alopecia
 It is an androgen-dependent, genetically determined
progressive disorder.
 Gradual conversion of terminal hairs into indeterminate
hairs and finally to vellus hairs.
 Patients with androgenetic alopecia have a reduction in
the terminal-to-vellus hair ratio, normally about 8:1.
 Androgenetic alopecia is essentially a cosmetic
disorder, also increases chances of actinic damage.
 It affects 50% of males.
 It has significant effect on the quality of life, more on
women.

34. Norwood Hamilton classification of Androgenic Alopecia

35. Etiology
In male
 Male balding is an androgen-dependent trait.
 Caused by dihydrotestesterone which has greater affinity for
androgen-receptors.
In women;
 Feature of hyperandrogenism, when accompanied by signs
of androgen excess hirsutism, ammenorrhoea, raised
circulating testesterone.
 Should search for androgen-secreting tumors

36.  The frontal hairline is often preserved in women with this
disorder, whereas men note a gradual recession of the
frontal hairline.
 Manifests in teens, 20’s, 30’s.
 Loss of hair chiefly from vertex, fronto-parietal region.
 Early onset is related to androgen-receptor gene & inherited
factors

37. Androgenic alopecia in women :
 There is diffuse hair loss through the apical scalp with
sparing of frontal hairline.
 Due to genetic pre-disposition with excessive response to
androgen.

39. Findings in Trichogram :
 In acute telogen effluvium, a reversal of the normal
anagen-to-telogen ratio can be seen.(Normal 8:1)
 Miniaturization of the hair shafts and low terminal
to-vellus hair counts are seen in androgenetic
alopecia.
 Characteristic peribulbar lymphocytic inflammation
can be seen in alopecia areata.

40. MANAGEMENT:
 Educating the patient about the natural history of the
condition is an imp aspect.
 The normal hair cycle should be explained, as well as the
relationship between triggers and the timing of hair loss.
 The patient should be instructed to record any stresses,
hospital admissions, surgical procedures, new medications,
dosage changes, or other potential triggers of hair loss.
 If the trigger is identified & removed , regrowth can be noted
in 3-6 months.

41.  Nutritional deficiencies, thyroid disease, systemic
illnesses, and infections should be treated.
 Biotin and zinc replacement can support hair
regrowth.

42. Treatment of Androgenetic Alopecia :
 Caution against unrealistic expectations; primary goal is to halt
progression.
 Male pattern hair loss
 5% topical minoxidil solution or foam twice daily.
 Oral finasteride, 1 mg daily.
 Combination of the above: Use for at least 6 months to assess
response, and continue treatment to maintain response.
 Surgery (e.g., hair transplantation). Most useful for restoring
frontal hair loss.

43.  Female pattern hair loss
 2%-5% topical minoxidil solution twice daily.
 Topical 17β-estradiol (e.g., estradiol benzoate, 20-25 mg/mL
isopropanol).
 Oral anti-androgens (spironolactone, cyproterone acetate).
 Combination of the above: Use for at least 6 months to assess
response, and continue treatment to maintain response.
 Maintain serum ferritin > 40 µg/L.
 Hair transplantation in selected cases

44. Topical Minoxidil
 Minoxidil (2% for women, 2% or 5% for men)
promotes survival of dermal papillary cells,
prolongs the anagen growth phase and gradually
enlarges miniaturized follicles (vellus hairs) into
mature terminal hairs.
 Best in early cases (<10 yrs), diameter <10 cm.
 Responds after 2-3 months
 Treatment is continued indefinitely because, once
treatment is stopped, hair loss resumes.

45.  The most frequent adverse effects are mild scalp
irritation, allergic contact dermatitis, and increased
facial hair.
 However, only 30-40% patients respond with
significant hair growth.

46. Combination and comparison with Minoxidil
 In a small study, finasteride 1 mg was superior to minoxidil 2
percent; this study also showed a trend toward better results
with combination therapy with finasteride and minoxidil
compared with finasteride alone.
Other options
 Surgery — Available procedures include hair transplantation or
flaps, and scalp reduction.
 Light therapy — Treatments with low-energy excimer laser light
 Patient education — Discourage use of hair treatments and
tonics; they are unproved, often expensive, and possibly
damaging to remaining hair.

47. Antiandrogens :
 Spironolactone (100-300 mg/day),flutamide (250-500 mg
twice or thrice a day),and cyproterone acetate (CPA 100
mg/day on days 5-15 of menstrual cycle and ethinyl estradiol
50 µg/day on 5-25 days,
 Finasteride inhibits the 5α-reductase enzyme, blocking
conversion of testosterone to dihydrotestosterone,
 1 mg po once/day can stop hair loss and can stimulate hair
growth. Efficacy is usually evident within 6 to 8 months of
treatment.
 Adverse effects include decreased libido, erectile and
ejaculatory dysfunction, hypersensitivity reactions,
gynecomastia

48. Treatment options for Alopecia areata
include :
 Topical,
 Intralesional, or,
 In severe cases, systemic corticosteroids,
 Topical minoxidil
 Topical anthralin
 Topical immunotherapy (Diphencyprone or squaric acid
dibutylester),
 or Psoralen plus ultraviolet A (PUVA).

50. Hair transplantation is a surgical technique that involves moving
skin containing hair follicles from one part of the body (the donor
site) to bald or balding parts (the recipient site).

52. D/D
 Trichotillomania
 Tinea capitis
 Traction alopecia
 Syphilitic alopecia

55. Interpreting Findings in Alopecia
Finding
 Asymmetric, bizarre, irregular hair loss
pattern
 Circular, discrete patches of loss; short,
broken hairs; exclamation point hairs at
periphery of patches
 Hair loss with a patchy, moth-eaten
appearance
 Pruritus, erythema, and scaling
 Pustules
 Scalp and body hair loss
 Unruly or unusually wooly hair
 Virilization
 Trichotillomania
 Alopecia areata
 Secondary syphilis
 Chronic cutaneous lupus
 Tinea capitis (particularly if adenopathy
present
 Scarring dermatologic or infectious process
(eg, dissecting cellulitis of the scalp, acne
keloidalis nuchae)
 Alopecia universalis
 Primary hair shaft abnormality
 Adrenal disorder or tumor
 Polycystic ovary syndrome
 Surreptitious anabolic steroid