This document discusses various types and causes of hair loss. It begins by classifying hair loss as scarring vs nonscarring, and diffuse vs localized. Nonscarring hair loss can be caused by telogen effluvium (the most common cause), anagen effluvium, androgenetic alopecia, etc. Triggers of telogen effluvium include stress, medical conditions, nutritional deficiencies, and certain drugs. Evaluation involves history, examination including pull test and trichogram, and basic lab tests. Treatment focuses on identifying and removing triggers when possible as well as medications for specific conditions like minoxidil for androgenetic alopecia.
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
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
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
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
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
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.
A discussion on various photodermatoses including sun burns, porphyria, actinic chelitis, hydroa vacciniforme and chronic actinic dermatitis. Sun tan and skin color types. Affect of Sunlight on the skin. Useful for medical residents, dermatologists and nurse. Useful in exam preparation.
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
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
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.
A discussion on various photodermatoses including sun burns, porphyria, actinic chelitis, hydroa vacciniforme and chronic actinic dermatitis. Sun tan and skin color types. Affect of Sunlight on the skin. Useful for medical residents, dermatologists and nurse. Useful in exam preparation.
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
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
Hair is an important part of who we are. The average person has 5 million hairs (100,000 – 150,000 are on the scalp). Blonds usually have more hair (about 140,000 hairs), brunettes have slightly higher than average hair (about 105,000 hairs), and redheads have a little less than average (about 90,000 hairs). Hair is composed of keratin, the same protein that nails and the outer layer of skin is made of. Hairs are produced by a small structure underneath the skin called the hair follicle.
Hair follicles are formed while we are still a fetus, and after we are born no new follicles are produced. Hair growth is often regulated by hormones within the body. At puberty, certain male hormones trigger the growth of pubic, underarm, and beard hairs. They can also trigger the start of genetic male pattern hair loss.
Each hair grows in a series of phases. In the growth phase, the hair is continually growing for up to five years. At the end of the growth cycle, there is a transitional phase where the hair does not grow and begins to change into the third phase. The third phase is the resting phase. During this phase, the follicle is no longer growing, and at the end the old hair is pushed out, then the cycle starts over and a new growth phase starts. This happens repeatedly throughout our lives, and is why even people unaffected with hair loss lose 50-100 hairs per day.
In people affected with genetic hair loss, there appears to be a higher number of hormone receptors in the areas of the scalp with hair loss. In most people affected by hair loss, male hormone levels are the same as in normal people, but because there are more receptors in the balding areas of the scalp they are affected as if their hormone levels were higher than normal. Researchers are still working on how the presence of a certain male hormone, Dihydrotestosterone (DHT), causes damage to follicles in people with genetic hair loss. As the follicles are damaged, the hairs grown are thinner and the growth cycles are shorter with each new growth cycle, until eventually no hair or a small, miniaturized hair is all that can be produced. As more and more hairs become smaller and more miniaturized, the person appears balder.
Genetic hair loss causes about 95% of all hair loss. Another main cause is an autoimmune condition known as Alopecia Areata (patchy hair loss), Alopecia Totalis (loss of all hair on the head), and Alopecia Universalis (loss of all hair on the body). Researchers are also working on a treatment for this condition. Other causes include hair loss due to side effects of medication, stress, or dietary deficiency.
Do you loose more than 100 hair a day? It is not normal.praveenkumar509531
Hair grows everywhere on the human skin except on places like the palms of hands and the soles of feet, eyelids and belly buttons. Hair is made up of a protein called keratin that is produced in hair follicles in the outer layer of skin.
Cicatricial Alopecia Hair Transplant, FUT Hair Transplant Surgery, hair transplant fue in Bangalore, alopecia areata treatment, alopecia areata cure, alopecia areata treatment in bnagalore, Alopecia Areata Causes, traction alopecia hair transplant, hair loss treatment for women, Hair Loss Treatment, Hair loss treatment for men, Hair transplantation (Transplant) FUT / FUE in Bangalore, Hair care in Bangalore, Hair Transplant Surgeon in Bangalore, Hair Transplant Surgeon in India, hair transplant after scarring alopecia
"Explore 'Allergy Treatment in Homeopathy'—uncover gentle yet powerful principles alleviating allergies naturally. Understand allergy roots, discover personalized remedies, and integrate homeopathy seamlessly into your wellness routine. Unravel the science and art of homeopathic allergy treatment, gaining knowledge and tools for a healthier, balanced life naturally. Join us on this transformative journey."
Hair loss alopecia baldness male pattern hair loss and homeopathy treatment a...Pranav Pandya
Hair loss, also known as alopecia or baldness, refers to a loss of hair from the head or body. Baldness can refer to general hair loss or male pattern hair loss
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
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)
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.
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
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.
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.
38.
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).
49.
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).