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Document Details

SelfSatisfactionHeliotrope9824

Uploaded by SelfSatisfactionHeliotrope9824

University of Duhok, College of Medicine

Dr. Mateen Ahmed Ali

Tags

hair disorders alopecia hair growth medical conditions

Summary

This document is a lecture or textbook on hair disorders. It covers various types of hair loss, including alopecia, and excessive hair growth like hirsutism. The document examines the causes, pathology, diagnosis, and treatments for different hair disorders.

Full Transcript

shedding orThinning LocalisedUdiffure in frontal is thinning Hypertichous 8 8 5 Hirsutism terminal traction OCD Localized Filipino Alopecia totalir Alopecia Un...

shedding orThinning LocalisedUdiffure in frontal is thinning Hypertichous 8 8 5 Hirsutism terminal traction OCD Localized Filipino Alopecia totalir Alopecia Universalis Lookitup pitting are regularunice in provrisis Allergic topical steroids oral FP ofidil I Look it up postmenopausal HAIR DISORDERS Dr. Mateen Ahmed Ali M.B.Ch.B C.A.B.D.V Lecturer in University of Duhok - College of Medicine Hair disorders Hair disorders is a broad category that includes the following conditions: Alopecia: the loss or thinning of hair. There are two types of alopecia: scarring, in which hair follicles are destroyed, and nonscarring, which can be reversed. The process of losing hair is called effluvium Male pattern baldness (androgenic alopecia): This is the most prominent type of hair disorder affecting, to varying degrees, half of all men over 50 years of age. Hirsutism: excessive male pattern hair growth affecting 8% of adult women. Hair shaft disorders: usually hereditary abnormalities. HAIR DISORDERS ALOPECIA DIFFUSE Phases of hair growth: 1. anagen: growth phase → 0.3 mm/day or 1 cm/month for 4-6 PATCHY (Localised) years (even wider range) (grows faster in children & summer 2. catagen: follicular regression where hair detaches from blood vessels → 2 weeks. Non scarring 3. telogen: resting phase → 3-4 months. exogen: extension of telogen where shedding occurs. scarring 1. Congenital 2. Acquired Localised (Patchy) hair loss Non- scarring 1. Neonatal hair loss 2. Early treated pyogenic or fungal infections 3. Traumatic alopecia A-Neonatal frictional alopecia B- Trichotillomania C-Traction alopecia D- Alopecia and lichen simplex 4. Alopecia Areata Scarring Alopecia Developmental defects and hereditary disorders Physical/chemical agents Burns Infections: a- bacterial b- Fungal c- Viral d- Prtozoal Neoplasms Miscellaneous: Lupus erythematosus: chronic cutaneous, Lichen planus, pseudopelade, Scleroderma/morphea Lichen planopilaris Diffuse hair loss 1-Androgenetic alopecia (common baldness) 2- Congenital: like ectodermal dysplasia 3-Alopecia areata (Diffuse form) 4- TELOGEN EFFLUVIUM 5- Metabolic and endocrine disorders 6- Nutritional deficiency 7- Drugs and chemicals: ANAGEN EFFLUVIUM 8-Chronic illnesses 9- Chronic diffuse alopecia of unknown origin 10- Hair shaft abnormality Telogen vs Anagen effluvium Telogen effluvium: delayed onset of hair loss because of their early entry from anagen to telogen phase as a result of paychological stress (e.g bereavement) or physiological stress (e.g COVID 19), so the hair would shed few months after the insult. Anagen effluvium: abrupt loss of hairs that are in their growing phase (anagen) due to an event that impairs the mitotic or metabolic activity of hair follicle. Drugs: systemic chemotherapy (esp. alkylating agents), anticoagulants, antidepressants. Radiation therapy to the scalp ALOPECIA AREATA Alopecia totalis Alopecia universalis “Exclamation-mark" Pigmentary changes Narrower at scalp Dystrophy, pigmentation Nail changes Aetiology 1. genetic factors 2. Immunological factors 3. Psychological factors 4. Significant association with atopic state and Down syndrome Course and prognosis The bad prognostic signs in alopecia areata 1- Alopecia areata in atopic patient. 2- Rapid progression. 3- The loss of eye brows and eye lashes. 4- Sever nail changes (Nail pitting, dystrophy and pigmentation 5- Ophiasis (the loss of hair of back and sides of scalp ) 6- Loss of hair in reticular pattern. 7- Alopecia totalis and universalis 8- Family history of atopy or alopecia areata. 9- Early onset before puberty. Treatment: Irritants like phenol, salicylic acid, resorcinol, garlic or other plant extracts to stimulate hair growth. Potent topical or Intralesional steroids. Chemical sensitizers like di-nitrochlorbenzene or squaric acid dibutylester to stimulate allergic contact dermatitis. Psoralen and ultraviolet light "PUVA" Topical Minoxidil. Anthralene (Dithranol) topical in short contact in 1-3% Immunomodulators like BCG vaccination, oral zinc sulphate or ionosiplex. Psychotherapy in anxious patients Androgenetic Alopecia (common baldness) Etiology – Shorter/thinner hair shafts Hair follicle undergoes stepwise miniaturization and change in growth dynamics Shorter anagen phase DHT believed to be primary repressor of hair growth Rate of progression and pattern appear to be genetically determined Signs/Symptoms – Androgenetic Alopecia - MEN Insidious in onset and usually does not start until after puberty Progression fluctuates considerably Occurs at top rear of head (vertex), frontal hairline, occipital regions Begins w/recession of frontal hairline, continues w/thinning at vertex Signs/Symptoms – Androgenetic Alopecia - WOMEN Hair loss more diffuse (thinning) Characteristic retention of frontal hairline Hair density remains normal but hair length does not Treatment Medical treatment: in female, antiandrogens like cyproterone acetate, spironolactone, or contraceptive pills Finastride can be used in male Or post-menopausal women because it is teratogenic for male fetus Minoxidil Specifically for loss of vertex but not frontal hair Increases cutaneous blood flow directly to hair follicles, which increase in size after treatment 2% conc. recommended for women 5% conc. recommended for men Should see growth in 4 mos (2%) or 2 mos (5%) Available as spray, dropper, rub-on Hair density returns to pretreatment levels after discontinuation Efficacy may be enhanced with finasteride 1mg Surgical treatment: by hair transplantation or scalp reduction Excessive hair growth Hirsutism Hirsutism is growth of terminal hair in females in androgen- dependent hair patterns secondary to increased androgenic activity Pathophysiology 50 % to 70 % of circulating testosterone in normal women is derived from adrenal or ovarian Testosterone precursors 99% of testosterone is found in the inactive or bound- form 5-α-Dihydrotestosterone, derived from conversion of androgen receptor bound testosterone, by 5- α- reductase enzyme Etiology 1. Adrenal Causes 2. Ovarian Causes 3. Exogenous Medications 4. Pitutary Causes 5. Ectopic virilizing Tumors 6. Idiopathic or undetermined Causes A- minor dysfunction of the adrenals. B- minor dysfunction of the ovaries. C- more active 5- α-reductase enzyme. D- Androgen receptors in the hair follicles are either large in number or oversensitive Investigations 1.U/S examination: may show polycystic ovaries 2. FSH and LH 3. Testosterone level: if very high may indicate virilizing tumor. 4. sex-hormone binding globulin. 5. other hormones: Prolactin growth hormone….etc. 6. 24 hours urine for steroids. 7. Skull x-ray or CT scan for pituitary causes Management A- Cosmetic Shaving, Hair epilation by thread, or waxing. Chemical depilation using calcium hydroxide or thioglycolate to destroy the hair above the hair surface. hydrogen peroxide bleaching All the above methods have temporary effect. electrolysis, thermolysis and Laser hair epilation Vaniqa: Eflonithine HCL topical cream B- Systemic Antiandrogen Therapy 1. Cyproterone Acetate (CPA) 2. SPIRONOLACTONE 3. CIMETIDINE 4. CORTICOSTEROID 5. ORAL CONTRACEPTIVES 6. KETOCONAZOLE 7. 5- α-reductase blockers like Finastride 8. more recently flutamide Hypertrichosis: Hypertrichosis is excessive hair growth that is coarser, longer, or more profuse for the patient age, race and sex also in areas that are not androgen-sensitive. Causes: 1. Localised Hypertrichosis A- Congenital: B- Acquired 2. Generalized Hypertrichosis: A- Congenital: 1. Congenital Hypertrichosis Lanuginosa 2. Foetal alcohol syndrome 3. Foetal hydantoin syndrome B- Acquired: 1.Acquired Hypertrichosis Lanuginosa 2. Associated with certain syndrome like glycogen storage disease. 3. Endocrine problems 4. Connective tissue diseases especially dermatomyositis. 5. Anorexia nervosa and other causes of malnutrition. 6. Head injury or encephalitis. 7. Drugs: Diphenylhydantoin: Diazoxide, Minoxidil, Cyclosporine, Streptomycin, Oral corticosteroids, Penicillamine, Psoralens Hair Colour Changes: 1. Hereditary variation 2. Graying of the hair 3. Poliosis 4. Nutritional deficiency Zinc deficiency: lead to blond hair. Kwashiorkor disease: Flag sign 5. Metabolic causes 6. Drugs 7. Alopecia areata 8. Premature canities 9. Cosmetic Hair coloring

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