This document provides information on skin anatomy, various benign dermatologic conditions, and treatments for skin conditions. It discusses the layers of the epidermis and dermis. It also describes common benign conditions like contact dermatitis, atopic dermatitis, acne, rosacea, psoriasis, nevi, and alopecia. For each condition, it discusses pathogenesis, clinical features, diagnosis, and management approaches including medications, procedures, and lifestyle changes.
1. Structure of skin.
2. Skin relating problems :
a. Dry skin
b. Acne
c. Pigmentation
d. Prickly heat
e. Wrinkles
f. Body odour
3. Structure of hair.
4. Hair growth cycle.
1. Structure of skin.
2. Skin relating problems :
a. Dry skin
b. Acne
c. Pigmentation
d. Prickly heat
e. Wrinkles
f. Body odour
3. Structure of hair.
4. Hair growth cycle.
Skin pigmentation:
Pigmentation means coloring. Skin pigmentation disorders affect the color of your skin. Your skin gets its color from a pigment called melanin. Special cells in the skin make melanin. When these cells become damaged or unhealthy, it affects melanin production. Some pigmentation disorders affect just patches of skin. Others affect your entire body.
For more information, you can book an appointment at
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
• Google+ link: https://goo.gl/vqAmvr
• Facebook link: https://goo.gl/tui98A
• Youtube link: https://goo.gl/mk7jfm
• Linkedin link: https://goo.gl/PrPgpB
• Slideshare link : http://goo.gl/0HY6ep
• Twitter Page : https://goo.gl/tohkcI
• Instagram page : https://goo.gl/OOGVig
Structure of skin relating to problems like dry skin, acne vulgaris, pigmenta...Jaswanth Gowda BH
This single presentation contains a complete information about structure of skin and its relating to problems such as dry skin, acne vulgaris, pigmentation, prickly heat, wrinkles, body odour, structure of hair and hair growth cycle, oral cavity problems.
This is a seminar conducted by 4th year medical student under supervision of a lecturer. Sorry for not attaching the references.
Information were from few textbooks, google and also from previous dermatology posting group's seminar.
Multi-factorial disease characterized by abnormalities in sebum production, follicular desquamation, bacterial proliferation and inflammation.
Acne vulgaris is a disease of the pilosebaceous follicle characterized by non-inflammatory (open and closed comedones) and inflammatory lesions (papules, pustules, and nodules)
Asked questions concerning acne.
How does acne develops ?
Factors for development of acne
What are the predisposing factors
Is it familiar? Is it controllable.
Is it associated with diet or dust?
Does cosmetics cause acne.
Does drugs cause acne.
Does stress has any role in causation of the acne
Acne is a dermatological problem affected by an estimated 65 million people worldwide. This presentation is based on the changes on the skin in relation to the problem 'acne'.
Skin pigmentation:
Pigmentation means coloring. Skin pigmentation disorders affect the color of your skin. Your skin gets its color from a pigment called melanin. Special cells in the skin make melanin. When these cells become damaged or unhealthy, it affects melanin production. Some pigmentation disorders affect just patches of skin. Others affect your entire body.
For more information, you can book an appointment at
Dr Sachdeva's Dental Aesthetic And Implant Institute,
I 101, Ashok Vihar Phase 1, Delhi- 110052
Contact us at
• Phone : +919818894041,01142464041
• Our Websites:
• www.sachdevadentalcare.com
• www.dentalclinicindelhi.com
• www.dentalimplantindia.co.in
• www.dentalcoursesdelhi.com
• www.facialaestheticsdelhi.com
• Google+ link: https://goo.gl/vqAmvr
• Facebook link: https://goo.gl/tui98A
• Youtube link: https://goo.gl/mk7jfm
• Linkedin link: https://goo.gl/PrPgpB
• Slideshare link : http://goo.gl/0HY6ep
• Twitter Page : https://goo.gl/tohkcI
• Instagram page : https://goo.gl/OOGVig
Structure of skin relating to problems like dry skin, acne vulgaris, pigmenta...Jaswanth Gowda BH
This single presentation contains a complete information about structure of skin and its relating to problems such as dry skin, acne vulgaris, pigmentation, prickly heat, wrinkles, body odour, structure of hair and hair growth cycle, oral cavity problems.
This is a seminar conducted by 4th year medical student under supervision of a lecturer. Sorry for not attaching the references.
Information were from few textbooks, google and also from previous dermatology posting group's seminar.
Multi-factorial disease characterized by abnormalities in sebum production, follicular desquamation, bacterial proliferation and inflammation.
Acne vulgaris is a disease of the pilosebaceous follicle characterized by non-inflammatory (open and closed comedones) and inflammatory lesions (papules, pustules, and nodules)
Asked questions concerning acne.
How does acne develops ?
Factors for development of acne
What are the predisposing factors
Is it familiar? Is it controllable.
Is it associated with diet or dust?
Does cosmetics cause acne.
Does drugs cause acne.
Does stress has any role in causation of the acne
Acne is a dermatological problem affected by an estimated 65 million people worldwide. This presentation is based on the changes on the skin in relation to the problem 'acne'.
The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions.
Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier
Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups.
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.
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.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
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.
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
5. • Specialized regions of skin, including the palms, soles, genitalia and scalp, have modified
forms that address
• Regional functional requirements
6. • The skin represents
the largest organ of
the human body.
• The skin serves as an
important interface to
the external
environment as both a
physical and an
immunologic barrier.
9. • UV radiation that reaches
the earth’s surface is
UVA and UVB.
• 95% is in the form of
UVA
• link of sun exposure
history (UV) and skin
cancer
10. Sunscreen
• UVB absorption by DNA results in a p53 tumor suppressor gene mutation
• UVB exposures over time have been associated with the formation of basal cell
carcinoma and melanoma.
• UVA absorption by DNA results information of oxygen free radicals
• UVA exposure has been linked to the development of melanoma in animal models
11. Sunscreens protect the skin either chemically or physically.
• Chemical sunscreens absorb UV (usually UVB) radiation with
the most common sunscreen ingredient being para-aminobenzoic
acid (PABA), benzophenones, and cinnamates.
• Physical sunscreens work by reflecting UV radiation and
producing a protective barrier. They are usually opaque and
include agents such as zinc oxide and titanium dioxide.
12. SPF (Sun Protection Factor) is a measurement of UVB protection only
SPF 30 blocks 97% for 2 hours
Tips
Apply 30 min prior and every 2 hr
13. Chemical Peels
• Application of solution to the skin surface
• Sol improve fine lines, acne scars, Wrinkles,
Skin discoloration
• Not for loose skin or very wrinkles and
scars
Thirty-one-year-old female with melasma
14. • Superficial peels cause exfoliation of the epidermis without deeper penetration.
• Medium peels affect the epidermis and penetrate into the papillary dermis,
• Deep peels penetrate into the reticular dermis where they cause realignment of
collagen.
15. • Peels are used for a wide variety of skin conditions ranging from
management of photodamage and melasma to hyperpigmentation,
rosacea, and acne.
• Deeper peels tend to have more profound and longer-lasting effect
compared with superficial peels.
16. • Superficial peels include glycolic acid and salicylic acid,
• Medium peels TCA (20%–35%) and Jessner’s
• Deep peels Phenol and TCA (45%–50%).
• Peels are commonly used in conjunction with other skin resurfacing modalities for improved
outcomes.
17. Laser Resurfacing
• Laser resurfacing relies on the principles of selective thermal destruction
(photothermolysis) to disrupt damaged areas of skin and to induce remodeling
24. Botulinum Toxin
• The most popular dermatologic uses of
BTX
• Works by causing temporary block in the
nerve signals preventing contraction of
muscles
• Approximately last for 3 months
31. • Contact dermatitis is an eczematous
dermatitis caused by exposure to
substances in the environment.
• Those substances act as irritants or
allergens and may cause acute, subacute,
or chronic eczematous inflammation.
1 Contact Dermatitis
32.
33. • Irritant contact dermatitis (ICD)
accounts for 80% of all contact
dermatitis
• The classic picture of contact
dermatitis is a
• well demarcated
• erythematous
• vesicular and/or scaly patch or
plaque with well-defined margins
corresponding to the area of contact
34. Management of Irritant Contact Dermatitis
1. Avoid exposure to irritants by using protective
equipment, such as gloves.
2. Topical steroids are used to initially control
inflammation but there is some evidence that they
may compromise barrier function. Some experts
recommend that the use of topical steroids should be
avoided.
Bilateral irritant contact
dermatitis of the palms
secondary to repeated contact
with paint solvents.
35. 3. Moisturizers used generously and
frequently increase skin hydration, and
their lipid component improves the
damaged skin barrier. Lipid-rich
moisturizers both prevent and treat irritant
contact dermatitis.
4. Barrier creams containing dimethicone or
perfluoropolyethers, cotton liners, and
softened fabrics prevent irritant contact
dermatitis.
Bilateral irritant contact dermatitis of the feet
and ankles due to chronic occlusive
footwear.
36. 5. Cool compresses are used for acute inflammation. They suppress vesiculation
and decrease inflammation.
6. Hands should be washed in cool or tepid water.
7. Repeated low-level ultraviolet (UV) exposures may be effective for long-term
resistant cases.
8. Even after the skin appears normal, it takes approximately 4 months or more for
barrier function to normalize.
37. Nickel allergy
Management of Allergic Contact Dermatitis
1. Minimize products for topical use.
2. Use ointments instead of creams (creams contain
preservatives and are complex mixtures of chemicals).
3. Botanical extracts may be used in “fragrance-free”
products.
4. When patch testing, also test the patient’s consumer
products.
5. Read product labels carefully. Many “dermatologist
recommended” products contain sensitizers (e.g.,
lanolin, fragrance, quaternium-15, parabens,
methylchloroisothiazolinone/methylisothiazolinone).
38. Cosmetic and fragrance allergies
Allergic contact dermatitis
occurred after application of
aftershave lotion.
39. • Irritant Contact Dermatitis and Allergic Contact Dermatitis are not always
discernible clinically, patch testing is required to help identify an allergen
• Patch testing is not useful as a diagnostic test for
irritant contact dermatitis because irritant
dermatitis is a non-immunologically mediated
inflammatory reaction.
40. Sites of specific patch tests labelled for
future reference following removal of the
chambers.
41. 2 Atopic Dermatitis
• Atopic dermatitis is a chronic, pruritic inflammatory
skin condition that typically affects the face (cheeks),
neck, arms, and legs but usually spares the groin and
axillary regions.
• AD usually starts in early infancy, but also affects a
substantial number of adults
• AD is commonly associated with elevated levels of
immunoglobulin E (IgE).
42. Clinical Features
• Xerosis (dry skin)
• Lichenification (thickening of the skin and an
increase in skin markings)
• Eczematous lesions (skin inflammation)
• Pruritus Early age of onset IgE reactivity
• Peripheral eosinophilia
• Staphylococcus aureus superinfection
44. • It may be accompanied by other disorders such as allergic rhinitis, asthma, food allergies,
and more rarely eosinophilic esophagitis.
45.
46. 3 Acne
• Acne represents a common dermatologic
condition affecting the pilosebaceous units and
typically presents in adolescence.
• Acne lesions favor the face, neck, upper back,
chest, and upper arms.
47. Pathogenesis
• The development of acne involves the interplay of a
variety of factors, including:
• (1) follicular hyperkeratinization;
• (2) hormonal influences on sebum production
and composition
• (3) inflammation, in part mediated by P. acnes
• Anatomy and Physiology of the pilosebaceous unit
is essential to understanding the pathogenesis of
acne and designing effective treatment regimens.
48.
49. Clinical Features
• Acne is typically found in sites with well-developed sebaceous glands, most often the face
and upper trunk
• Acne lesions are divided into non-inflammatory and inflammatory groups based upon their
clinical appearance.
52. Epidemiology
• Incidence and age: predominantly a disorder of
adolescence; affects 85% of individuals between 12 and 24
years of age; may affect all age groups
• Race: lower incidence in African-Americans and Asians
• Sex: more severe forms in males
55. 4 Rosacea
• Chronic vascular and acneiform disorder of the pilosebaceous unit
56. Clinical features
• Facial flushing
• Telangiectasia
• Coarseness of skin
• Inflammatory papulopustular
eruption resembling care
• Nonpitting facial edema with
erythema
57.
58. Rosacea was classified into four clinical subtypes
• Erythematotelangiectatic
• Papulopustular
• Phymatous
• Ocular
59. Etiology
• Unknown
Several Factors
• Vasculature
• Pilosebaceous unit abnormalities
• Climate exposures
• Dermal matrix degeneration
• Chemical and ingested agents
• Microbial organisms
• Ferritin expression
• Reactive oxygen species(ROS)
• Increased neoangiogenesis
60. Management
• Patient education for skin care
• Topical
• Metronidazole (0. 75%-1 % ) once or twice daily,
• 10% sodium sulfacetamide with 5 % sulfur once daily, and
• azelaic acid once daily
• Systemic
• Tetracycline
• Doxycycline
• Oral isotretinoin
• Surgical
61. 5 Psoriasis
Is a chronic, complex, multifactorial, inflammatory disease
that involves hyperproliferation of the keratinocytes in the
epidermis, with an increase in the epidermal cell turnover rate.
62. Clinical finding
• Worsening of a long-term erythematous scaly
area
• Sudden onset of many small areas of scaly
redness
• Recent streptococcal throat infection, viral
infection, immunization, use of antimalarial
drug, or trauma
• Family history of similar skin condition
• Pain Dystrophic nails Long-term rash with
recent presentation of joint pain
63. • The pathogenesis of this disease is not completely understood
• Environmental, genetic, and immunologic factors appear to play a role.
65. Systemic Treatment
• Methorexate
• Retinoids, predominanetly acitretin
• Cyclosporine
• Biologics such as alefacept, etanercept, efaluzimab, and infliximab
Laser and Light Treatments
• Psoralen with Ultraviolet A
• Ultraviolet B (UVB), 311-nm narrowband-UVB (NBUVB)
• 308-nm UVB excimer laser
66. • Nevi are benign tumors composed of nevus cells
that are derived from melanocytes.
• The incidence peaks in the fourth to fifth
decades.
• They are present in 1% of newborns
Large congenital hairy nevus.
6 Nevi ( Benign Melanocyte Proliferation )
67. Common acquired melanocytic nevi include:
• Junctional nevi: where there is proliferation of the melanocytes at the dermal-
epidermal junction
• Compound nevi: with both intraepidermal and intradermal complexes of
melanocytes
• Intradermal nevi: with the melanocytes being located in the dermis
68.
69. Differentiating these from malignant melanoma can be
difficult
• The ABCDE pneumonic
Asymmetry
Border irregularity
Color variation
Diameter
Enlarging or evolving
70.
71. Treatment
• Risk assessment and treatment options are considered for each patient.
• Medical and psychosocial concerns need to be discussed.
• Management goals are to decrease the risk for developing melanoma by
surgical removal and to produce good cosmetic results.
• Electrocautery should be avoided
• Most common nevi are small and shave excision is adequate.
72. • Timing of surgery is a consideration.
• The best surgical scars result from surgery performed early in life; however, it may be
best to delay surgery until after age 2 when the full extent of the nevus is evident.
• Very large lesions may require multiple procedures.
• Should be removed down to the fascial layer.
73. 7 Alopecia and Hair Disorder
• The causes of hair loss (alopecia) are numerous.
• Most hair problems seen by the practitioner are due to changes in hair-follicle
cycling.
• Many inflammatory conditions permanently damage the hair follicle, resulting in
scarring alopecia.
• Alopecia can be the result of hair follicle loss, loss of the hair shaft, or a
combination of both.
75. Generalized Hair loss
Telogen Effluvium
A number of events have been documented that prematurely terminate
anagen and cause an abnormally high number of normal hairs to enter the resting, or
telogen, phase
• The follicle is not diseased
• Scarring and inflammation are absent.
Resting hairs on the scalp are retained for approximately 100 days before
they are lost; therefore telogen hair loss should occur approximately 3 months after
the event that terminated normal hair growth.
76. CAUSES OF TELOGEN EFFLUVIUM
• Shedding of the newborn (physiologic)
• Postpartum (physiologic)
• Chronic telogen effluvium (no attributable cause or illness)
• Postfebrile (extremely high fevers, e.g. malaria)
• Severe infection
• Severe chronic illness (e.g. HIV disease, systemic lupus erythematosus)
• Severe, prolonged psychological stress
• Postsurgical (implies major surgical procedure)
77. • Hypothyroidism and other endocrinopathies (e.g. hyperparathyroidism, hyperthyroidism)
• Crash or liquid protein diets; starvation/malnutrition
• Drugs:
- discontinuation of oral contraceptives
- retinoids (acitretin, isotretinoin) and vitamin A excess
- anticoagulants (especially heparin)
- antithyroid (propylthiouracil, methimazole)
- anticonvulsants (e.g. phenytoin, valproic acid, carbamazepine)
- interferon-α-2b
- heavy metals
- β-blockers (e.g. propranolol)
78. • Many physicians test patients with hair loss for iron
deficiency and thyroid abnormalities. Iron deficiency is
commonly found in CTE but treatment for it seldom reverses
the hair loss.
• Treat with 5% minoxidil solution.
79. Localized Hair Loss
Androgenic alopecia (Male Pattern Hair Loss)
• Androgenic alopecia represents one of the
most common acquired forms of hair loss
• Baldness in men is not a disease, but rather a
physiologic reaction induced by androgens in
genetically predisposed men.
• Thinning of the hair begins between the ages
of 12 and 40 years
80. Epidemiology
• Incidence: 30% of males older than 30 years; more than half of males older than
50 years .
• Age: begins after puberty.
• Precipitating factors: polygenetic inherited predisposition .
• No diagnostic tests exist to determine the etiology and natural progression .
81. Pathogenesis
• Androgens, in particular testosterone and
dihydrotestosterone (DHT), are required for the
progressive reduction in hair follicle size with each
cycle.
• Androgenetic alopecia is due to the progressive
shortening of successive anagen cycles.
• There are two populations of scalp follicles: androgen-
sensitive follicles on the top and androgen-independent
follicles on the sides and back of the scalp.
84. Low Level Light Therapy
(LLLT)
• In 2007, a low level light
device was approved by the
U. S. Food and Drug
Administration ( FDA) to treat
male pattern hair loss
85. Hair Transplantation Procedure
Trim donor region with moustache trimmer, and tape hair
up so donor suture will not be visible in the postoperative
period
Donor strip should not be more than 1 cm wide. Strips >1 cm
have an increased risk of creating a hypertrophic scar
86. Magnification helps visualize 1 to 4 hair bundles and minimize
transection when separating with surgical prep blades
93. • Topical minoxidil (2% and 5% solution) are the only medications for female
pattern hair loss approved by the U . S . Food and Drug Administration
94. Female pattern hair loss in a 10-year-old girl. A Prior to treatment.
B Obvious improvement following 5 years of therapy with oral
spironolactone and topical minoxidil