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Soutor 1e- Clinical Dermatology- Lecture 9- Hair, Nail and Pigment Disorders
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Soutor 1e- Clinical Dermatology- Lecture 9- Hair, Nail and Pigment Disorders
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Language: EN.
Segment:0 .
Segment:1 1. Hair, Nail, and Pigment Disorders.
DR. HORDINSKY: Hello, I am Dr. Maria Hordinsky, Professor and Chair of the Department of Dermatology at the University of Minnesota Medical School in Minneapolis.
Segment:2 2. Learning Objectives.
DR. HORDINSKY: In this presentation, we will cover common presentations of the nonscarring alopecias or hair disorders, the scarring alopecias, nail disorders, and disorders which cause hyper and hypopigmentation of the skin.
Segment:3 3. Hair Disorders: Two Major Categories.
DR. HORDINSKY: Hair disorders are categorized into two major categories: the nonscarring alopecias and the scarring or cicatricial alopecias.
DR. HORDINSKY: There are three major nonscarring alopecias: androgenetic alopecia or hereditary balding which can occur in both males and females, alopecia areata and telogen effluvium. The major scarring or cicatricial alopecias include the lymphocytic cicatricial alopecias, the neutrophilic ones, and mixed cicatricial alopecias.
Segment:4 4. History Questions for the Patient with the Chief Complaint of Scalp Hair Loss.
DR. HORDINSKY: For the patient who presents with the chief complaint of scalp hair loss, ascertain if this complaint is truly loss or is it hair thinning.
DR. HORDINSKY: Is there or isn't there increased shedding? Review hair care habits as well as prescription and nonprescription medications such as supplements, herbals, botanicals or use of any other chemicals. Ask about symptoms such as pain, itch and burning, and whether or not there is a hair care product relationship with a symptom. Check on body hair. Is there too much or too little?
DR. HORDINSKY: Are there nail abnormalities? Review the family history for hair diseases. Ask about signs of androgen excess or a history of autoimmune or endocrine diseases. Check for recent or chronic illnesses as well as recent surgical procedures. And for females, query about the menstrual cycle and pregnancies.
Segment:5 5. Examination of the Patient with the Chief Complaint of Scalp Hair Loss.
DR. HORDINSKY: The examination of the patient who presents with the chief complaint of scalp hair loss is as follows.
DR. HORDINSKY: First, closely examine the scalp. Look for and document the presence or absence of the following: erythema or redness, scale, folliculitis or scarring. Look for evidence of new hair growth. These will be fibers with tapered ends. Also look for hair breakage which could be congenital or related to poor haircare habits. Perform a pull test to assess for active shedding.
DR. HORDINSKY: Also note body hair density and distribution. Document any nail abnormalities, and for classification, one can use scales such as the Ludwig for females, Hamilton-Norwood for male pattern alopecia, the SALT score for alopecia areata or the Ferriman-Gallwey scale to define hirsutism.
Segment:6 6. Laboratory Tests.
DR. HORDINSKY: When evaluating the patient with hair loss, basic laboratory tests are usually ordered.
DR. HORDINSKY: These include thyroid stimulating hormone and a complete blood count, ferritin and iron profiles, particularly in women. If indicated by the history and physical examination, hormones such as DHEA-S, dehydroepiandrosterone sulfate and total and free testosterone can be checked. An antinuclear antibody and other autoantibodies could also be ordered if indicated by history and physical examination.
DR. HORDINSKY: If there is a question about poor nutrition or oversupplementation, zinc, vitamin D, vitamin A, vitamin E and total protein may be checked.
Segment:7 7. Androgenetic Alopecia.
DR. HORDINSKY: Androgenetic alopecia, also known as pattern balding, is characterized by progressive miniaturization of terminal hairs or shortening of the growth phase of the hair follicle called anagen. Patients present with a patterned type of hair loss classified using the Hamilton-Norwood scale in males or the Ludwig scale in females.
DR. HORDINSKY: Androgenetic alopecia is considered to be an androgen-dependent trait with polygenic inheritance and variable penetrance.
Segment:8 8. Androgenetic Alopecia.
DR. HORDINSKY: On this slide in Figure 1 we see on the top the Hamilton-Norwood scale and on the bottom the Ludwig scale, and the different patterns of balding that may occur in men and women, respectively.
Segment:9 9. Male and Female Androgenetic Alopecia.
DR. HORDINSKY: Figure 2 is an example of a male with androgenetic alopecia who is demonstrating Hamilton type IV balding where the balding is primarily in the vertex region.
DR. HORDINSKY: Figure 3 is an example of a female with Ludwig II androgenetic alopecia with pattern thinning centrally and retention of the frontal scalp hairline.
Segment:10 10. Hirsutism.
DR. HORDINSKY: Hirsutism is defined as the presence of terminal hair growth which follows a similar pattern to that developing in androgen-dependent sites in men after puberty as shown in Figure 4. Hirsutism is frequently associated with alopecia in women or other signs of androgen excess such as acne.
DR. HORDINSKY: Hirsutism may be end-organ specific and limited to the hair follicle only, or it may be inherited or associated with ovarian or adrenal gland disease.
Segment:11 11. Alopecia Areata (AA).
DR. HORDINSKY: Alopecia areata is shown on this slide. Alopecia areata is a complex, genetic immune-mediated disease that targets anagen or actively growing follicles. The disease affects approximately 2% of the population.
DR. HORDINSKY: The disease may be limited and patchy as shown in Figure 5 or extensive patchy as shown in Figure 6, or patients may present with complete loss of body and scalp hair. In alopecia areata, the hair follicle is not destroyed and maintains its potential to regrow hair.
Segment:12 12. Telogen Effluvium.
DR. HORDINSKY: Telogen effluvium, another nonscarring alopecia, results from the premature conversion of anagen follicles, actively growing follicles, to telogen or resting follicles.
DR. HORDINSKY: A clinical example is shown in Figure 7. Telogen effluvium can be associated with many situations including the postpartum period, medications, weight loss, acute and chronic illness. Telogen effluvium may be acute or chronic, and when chronic may be associated with significant temporal thinning as shown in Figure 8.
Segment:13 13. Hair Follicle.
DR. HORDINSKY: A schematic of the hair follicle is shown on this slide. There is also a blue line that has been drawn.
DR. HORDINSKY: Inflammation below this line is seen in alopecia areata where the inflammation is around the bulb or peribulbar inflammation, and is not associated with permanent hair loss. In contrast, inflammation above the blue line around the bulge region is associated with scarring and permanent injury.
Segment:14 14. Cicatricial (Scarring) Alopecias.
DR. HORDINSKY: We will now turn to the cicatricial or scarring alopecias. Early stages of these hair disorders may be distinguished clinically, but the end stages are indistinguishable, and all are characterized by permanent injury and scarring.
DR. HORDINSKY: The scarring alopecias can be broadly characterized by their inflammatory infiltrates seen microscopically. This can be either lymphocytic, neutrophilic or mixed. Treatments of the cicatricial or scarring alopecias may arrest signs and symptoms and disease progression.
Segment:15 15. Examples of Lymphocytic Cicatricial (Scarring) Alopecias.
DR. HORDINSKY: On this slide, there are four examples of lymphocytic or cicatricial scarring alopecias. In the first three, lichen planopilaris, central centrifugal scarring alopecia, and frontal fibrosing alopecia, peripheral inflammation will be seen.
DR. HORDINSKY: In the fourth, discoid lupus erythematosus, the inflammation is present within the affected area. We will now review each of these conditions. Figure 10 is an example of lichen planopilaris where there is scarring present as well as perifollicular scale and inflammation. Figure 11 is an example of central centrifugal scarring alopecia which is characterized by central scalp scarring and extension to the temporal regions as well as peripheral inflammation.
DR. HORDINSKY: Figure 12 is an example of frontal fibrosing alopecia where one sees regression of the hairline with perifollicular inflammation at the active margin. Figure 13 is an example of discoid lupus erythematosus which differs from the others in that inflammation is present within the affected area along with hyperkeratosis and accentuation of the hair follicle orifices.
Segment:16 16. Examples of Neutrophilic Cicatricial (Scarring) Alopecias.
DR. HORDINSKY: Two examples of the neutrophilic cicatricial scarring alopecias are shown on this side.
DR. HORDINSKY: Figure 14 is an example of dissecting cellulitis also known as dissecting folliculitis. In this condition, there are nodules, boggy plaques with sinus tract formation and a scarring alopecia. Folliculitis decalvans is shown in Figure 15. In this condition, there are follicular papules, patchy scarring alopecia with crusting from draining pustules present.
Segment:17 17. Nail Anatomy (Figures 16 and 17).
DR. HORDINSKY: Figures 16 and 17 show the anatomy of the nail.
DR. HORDINSKY: It is important to understand the anatomy of the nail to understand nail disorders. We will briefly review the anatomy of the nail. The nail matrix is what forms the nail plate. The nail plate is the hard, translucent keratin-containing structure which covers the dorsal surface of the distal digits on the hands and feet and is formed by the nail matrix. The lunula is the small white semicircular structure at the proximal portion of the nail.
DR. HORDINSKY: The nail bed is the structure underlying the nail plate which contributes to the nail plate's ability to attach to the finger. The hyponychium is the transition point between the nail and the normal skin of the digits. The onychodermal band is the point of strongest attachment between the nail and the underlying digit. The cuticle protects the matrix by sealing off the potential space between the nail plate and the proximal nail fold.
Segment:18 18. Common Categories of Nail Disorders.
DR. HORDINSKY: There are five common categories of nail disorders. These include infectious, papulosquamous, traumatic, systemic and tumors.
Segment:19 19. Fungal Infections of the Nails.
DR. HORDINSKY: On this slide, fungal infections of the nails are presented. Dermatophyte infections are found in 2 to 13% of the population. Trichophyton rubrum is the most common organism and often occurs with tinea pedis. The disease presents with white, yellow, orange or brown patches under a thickened nail plate as shown in Figure 18 or as a chalky white nail plate as shown in Figure 19.
DR. HORDINSKY: The disease is usually chronic and progressive if not treated. Candida fungal infections of the nails also occurs, and may present with diffuse leukonychia, white spots under the nail plate. Molds may also infect the nails and are frequently seen with periungual infections.
Segment:20 20. Bacterial Infections of the Nails.
DR. HORDINSKY: Bacterial infections can also affect the nails as shown on this slide.
DR. HORDINSKY: Pseudomonas is a common colonizer of onycholytic nails and the nail is usually discolored green or black as shown in Figure 20. Affected patients often have a history of wetwork.
Segment:21 21. Papulosquamous Diseases of the Nails.
DR. HORDINSKY: Papulosquamous diseases of the nails are shown on this slide. Figure 21 is an example of psoriasis affecting the nails, and in Figure 22, the disease lichen planus. Psoriasis of the nails commonly presents with pitting, onycholysis or separation of the nail plate from the nail bed, subungual debris and discoloration as shown in Figure 21.
DR. HORDINSKY: Patients with nail involvement are more likely to have psoriatic arthritis. Psoriatic nails can be secondarily infected with a dermatophyte. Lichen planus commonly occurs in isolation without any evidence of skin or mucosal lichen planus. It presents abruptly with longitudinal ridging, thinning and fissuring of the nail plate and possible pterygium as shown in Figure 22.
Segment:22 22. Traumatic Nail Disorders.
DR. HORDINSKY: Traumatic nail disorders are shown in this slide. Figure 23 is an example of habit tic deformity. There are roughly parallel horizontal depressions often over the median nail plate. These are caused by picking, rubbing, or scratching the proximal nail fold or cuticle. Figure 24 is an example of onycholysis where the nail plate is detached from the nail bed. This may be caused by exposure to irritants or physical trauma.
Segment:23 23. Nail Findings in Systemic Disease.
DR. HORDINSKY: Nail findings can be seen in systemic disease. These include Beau's lines, clubbing, koilonychia or spoon nails, splinter hemorrhages, Terry's nails, and yellow nail syndrome. Beau's lines are horizontal, depressed, white, nonblanching bands in the nail plate. These can be caused by systemic insults, drugs or trauma. Clubbing is overcurvature of the nail. This can be idiopathic or related to cardiovascular, pulmonary or gastrointestinal disorders.
DR. HORDINSKY: Spoon nails or koilonychia where the center of the nail is depressed relative to the edges can be caused by iron deficiency, hypothyroidism, trauma or be congenital. by iron deficiency, hypothyroidism, trauma or be congenital. Splinter hemorrhages are small longitudinal lines of dark discoloration usually caused by trauma, but these can also be related to systemic illnesses or drugs. Terry's nails are nails which are white proximally with a narrow pink or brown distal band and can be related to liver disease or aging.
DR. HORDINSKY: Yellow nail syndrome is characterized by diffuse yellow thickened nail plates, and these are commonly seen in patients with lung disease and chronic lymphedema.
Segment:24 24. Pigment Disorders.
DR. HORDINSKY: We will now discuss pigment disorders. We will discuss vitiligo, melasma, postinflammatory hyperpigmentation, and postinflammatory hypopigmentation.
Segment:25 25. Vitiligo.
DR. HORDINSKY: Figure 25 is an example of vitiligo, a skin disease that affects up to 1% of the world's population.
DR. HORDINSKY: It is a progressive disease with onset frequently after age 20. It is considered to be an autoimmune disorder which can be associated with other autoimmune diseases such as hypothyroidism. Vitiligo presents with bilateral symmetrical depigmented patches, typically on the face, trunk and extremities as shown in Figure 25.
Segment:26 26. Melasma.
DR. HORDINSKY: Melasma is triggered by sunlight, pregnancy, oral contraceptives, and presents with tan to brown patches across the forehead, upper cheeks and upper lips as seen in Figure 26.
DR. HORDINSKY: It is commonly seen in women ages 20 to 50 who have darker skin tones, most frequently Fitzpatrick skin types III to VI.
Segment:27 27. Postinflammatory Hyperpigmentation.
DR. HORDINSKY: Postinflammatory hyperpigmentation is usually triggered by inflammation such as acne, dermatitis, or injury. Postinflammatory hyperpigmentation presents with hyperpigmented macules with indistinct borders as shown in Figure 27. Postinflammatory hyperpigmentation is most common in those with Fitzpatrick skin types IV through VI.
Segment:28 28. Postinflammatory Hypopigmentation.
DR. HORDINSKY: Postinflammatory hypopigmentation can be triggered by inflammation such as discoid lupus erythematosus as shown in Figure 28, atopic dermatitis or trauma. Postinflammatory hypopigmentation presents with hypopigmented to depigmented macules, and in some cases, the pigment loss may be permanent.
Segment:29 29. Summary.
DR. HORDINSKY: In summary, disorders of hair, nails and pigment are common. Hair diseases are heterogeneous and can be immune-mediated as seen is alopecia areata, regulated by androgens as seen in male or female androgenetic alopecia, or be associated with inflammation in the bulge region with resultant scarring as seen in the cicatricial alopecias.
DR. HORDINSKY: Nail diseases are also heterogeneous and can affect any major part of the nail unit. Pigment disorders are characterized by loss of pigment cells as in vitiligo, or pigment cell dysfunction as seen in melasma or postinflammatory hyperpigmentation.
Segment:30 30. Contributors.