Hair and Nails



Hair and Nails


Kim B. Sanders






NORMAL HAIR


I. OVERVIEW

A. Hair is a keratin structure of the epidermis and a specialized skin appendage. The physiologic functions include insulation, esthetic and cosmetic display, tactile perception, thermoregulation, and protection from UV light.

B. Embryonic development

1. First follicles form at about 9 weeks of gestation, mainly in the eyebrows, upper lip, and chin. Remainder develop at 4 to 5 months of gestation.

2. Epidermal cells progressively penetrate downward into the maturing dermis, passing through “germ,” “peg,” and “bulbous peg” stages of development.

3. No hair follicles form after birth.

C. Anatomy

1. The hair shaft is organized into seven longitudinal regions, beginning from the epidermis (Figure 22-1).

a. Hair canal region—present only during fetal development and extends from the skin surface to the level of the epidermal-dermal junction

b. Infundibulum—funnel-shaped top of follicular canal. Extends to opening of the sebaceous duct

c. Sebaceous gland area

d. Isthmus—located between the entry of sebaceous duct and insertion of arrector pili muscle

e. Area of the bulge—site of the insertion of the arrector pili muscle

f. Lower follicle—extends from the area of the bulge to the top of the hair bulb

g. Hair bulb—is the deepest part of the hair follicle and surrounds the dermal papilla

2. Cross section of hair follicle reveals a series of cellular compartments (Figure 22-2).

a. A cellular basement membrane (“glassy membrane”). Surrounds entire follicle

b. Outer root sheath—most peripheral of cellular components

c. Inner root sheath—comprised of three separate layers. From outermost to innermost:

(1) Henle layer

(2) Huxley layer

(3) Cuticle

d. Hair shaft—also comprised of three separate layers. From outermost to innermost:

(1) Cuticle—the outside portion. Consists of overlapping cell layers arranged like shingles, which protect the hair shaft.

(2) Cortex—the bulk of the hair shaft. “Cigar-shaped” cells, which synthesize and accumulate proteins while in the lower regions of the hair shaft.







FIGURE 22-1. Schematic drawing showing anatomy of the hair follicle. (From Schalock, P. C., et al. (2010). Lippincott’s primary care dermatology. Philadelphia, PA: Wolters Kluwer. Asset provided by Anatomical Chart Co.)

(3) Medulla—present only in large terminal hairs. May be discontinuous.

D. Hair growth

1. Hair growth is cyclical, and follicles grow in a repeated three-part cycle. Each follicle functions as an independent unit (Figure 22-3).

a. Anagen—actively growing hair. Can be subdivided into six stages. For scalp hair, lasts 2 to 7 years.






FIGURE 22-2. Cross-section of a hair follicle. (From Anatomical Chart Company, 2004.)

b. Catagen—metabolic processes associated with hair growth gradually decreasing. The hair follicle regresses. Can be subdivided into eight stages. Lasts approximately 2 to 3 weeks regardless of site and follicle type.

c. Telogen—the resting phase. Existing hair will never grow longer. Lasts 3 months for scalp hairs. Hairs have a club-shaped proximal end, which will be shed from the follicle during the telogen-to-anagen transition called exogen.

2. Length of growth cycle varies according to body site with a general relationship of increasing hair length to a longer growth cycle.

3. Genetic programs determine normal growth parameters for hair on different anatomical locations; for example, eyelash hairs remain short while scalp hair grows much longer.

4. Hormones influence hair growth. Androgens influence pubic, axillary, beard, trunk, and extremity hair as well as lead to hair loss in susceptible individuals. Estrogens tend to prolong the telogen phase and delay the anagen phase.

E. Distribution of hair

1. Covers entire body except palms, soles, interspaces of the digits, and portions of the genitalia.







FIGURE 22-3. The hair growth cycle. (From Anatomical Chart Company, 2004.)

2. Greatest density on scalp, numbering 100,000 in people with brown/black hair. Is about 20% greater in natural blondes and 20% less in redheads.

3. At any given time, 85% to 90% of hairs are in anagen, 10% to 15% are in telogen, and less than 1% are in catagen.

4. Normal hair shedding ranges from 50 to 100 scalp hairs per day.

F. Types of hair

1. Hairs are classified into four groups according to texture and length.

a. Lanugo hairs—soft, fine, lightly pigmented hair. Found in utero on fetal skin. These are shed between 32nd and 36th weeks of gestation.

b. Vellus hairs—fine, short hair with little pigment. Replace lanugo hairs. Found on all parts of body except palms, soles, parts of genitalia, and periungual areas.

c. Indeterminate hairs—fall between vellus and terminal hairs in size.

d. Terminal hairs—thicker, longer, coarser hair. Frequently has a central medulla and is pigmented. Found only on scalp, eyebrows, and eyelashes in children. Androgen production at puberty stimulates conversion from small to large terminal hairs in scalp, beard (males), axillary, and pubic regions.

2. Any one hair follicle can give rise to different types of hair within its lifetime; for example, during puberty, former vellus hairs become terminal hairs in the beard, scalp, pubic, and axillary regions.

G. Hair pigmentation

1. Melanocytes located in the hair bulb of the follicle produce pigment.

2. Pigment is most prominent in the cortex of the hair shaft.

3. Any follicle can produce two types of pigment, although usually only one type at any time is found.

a. Eumelanin—pigment found in brown or black hairs

b. Pheomelanin—pigment found in red or blonde hairs

4. Generally, pigment is not found in the hair shaft during the early stages of new hair formation and in the proximal portion of telogen hairs.

5. Color intensity is generally proportional to the amount of pigment in the fiber.

6. Graying hair is a result of a decreased number of melanocytes in the hair bulb.

H. Morphology of hair

1. Four categories: straight, spiral, helical, and wavy.

2. Caucasians are the hairiest and may contain any of these categories.

3. Asian hair is straight due to straight follicles with lower portions oriented vertically to the skin surface.

4. Hair in blacks is spiraled due to curved follicles with lower portions almost horizontal to the skin surface.


II. ASSESSMENT

A. History and physical examination

1. Patient history—cause may be associated with a variety of other diseases, which significantly affect treatment decisions. Pertinent history may include the following:

a. Hair change duration, age of onset, and extent of involvement including:

(1) Distinguishing between thinning and shedding

(2) Loss or gain, diffuse or focal

(3) Areas of hair loss, scarring or nonscarring

(4) Increase or decrease in amount of hair lost per day

(5) Change in color or texture

(6) Distribution of hair, normal or abnormal

(7) Gradual or sudden onset

(8) Symmetric or asymmetric hair loss

b. Associated symptoms may include pruritus, pain, skin lesions, fever, pregnancy, psychologic or physiologic stress, or presence of systemic disease.

c. Current medications and supplements


d. Exposure to environmental or occupational toxins or chemicals

e. Nutritional status

f. Current and past treatment and response

2. Physical examination—inspect hair for texture, color, quality, and distribution.

B. Diagnostic tests: when the diagnosis is not clinically evident, the following tests may be indicated.

1. Hair pull test

2. Microscopic examination of the hair

3. Hair counts

4. Biopsy

5. KOH preparation

6. Fungal culture

7. Immune, endocrine, and other laboratory studies, if indicated



HAIR DISORDERS: ALOPECIA AREATA


I. OVERVIEW

A. Definition: nonscarring alopecia with rapid and complete loss of hair in round patches. Usually involves the scalp, beard, eyebrows, and eyelashes. Chronic and relapsing.

B. Etiology

1. Cause unknown but likely a hair-specific autoimmune disease

C. Pathophysiology

1. Telogen and dystrophic hairs with irregular shapes and fractured ends are removed in hair pull tests.

2. Dystrophic hairs fracture forming “explanation point” hairs found at the edges of hairless patches.

3. Lymphatic infiltrate found around affected hair bulb and lower one third of follicle.

4. Hair cycle is disrupted and an increased number of terminal catagen and telogen hairs are present.

5. Normal total number of hair follicles.

6. Inflammatory insult to matrix causes tapering of hair shaft.

D. Clinical features

1. Classic presentation is a well-defined round or oval patch of total hair loss on the scalp. There are three less common subtypes:

a. Alopecia totalis—loss of all terminal scalp hairs

b. Alopecia universalis—loss of all scalp and body hair

c. Ophiasis—band of alopecia around the temporal and occipital scalp

2. Paresthesia or pruritus may accompany hair loss in some patients.

3. Disease activity may be insidious or rapid.

4. Scarring is not present, unless disease is long standing.

5. Nail findings may include pitting, thin or brittle fingernails and toenails, and longitudinal ridging.

6. With regrowth, the hairs may initially be gray or white, but eventually repigment.

E. Incidence

1. Affects males and females equally.

2. Occurs in both children and adults. However, 50% of cases occur before age 20.


II. ASSESSMENT

A. See Normal Hair, Assessment.

B. If prompted by symptoms, investigate possible disease associations such as:

1. Atopy (atopic dermatitis, allergic rhinitis, or asthma)

2. Autoimmune diseases such as thyroid disease, vitiligo, inflammatory bowel disease, or polyendocrinopathy

3. Emotional distress


III. COMMON THERAPEUTIC MODALITIES

A. Medical interventions

1. Intralesional corticosteroid injections, particularly on scalp or eyebrows. About 66% of patients will experience some growth.

a. Inject involved area with dilute triamcinolone acetonide suspension up to 10 mg/mL (scalp) or 3 to 5 mg/mL (eyebrows) using a 27- or 30-gauge needle.

b. Reinject at 4- to 6-week intervals. Discontinue after 3 months if no growth present.

c. Thinning of regrowth may occur after 3 to 6 months and can be reinjected as necessary.

d. Spontaneous regrowth may occur 3 to 6 months after injection.

2. Potent topical steroids. Short white or finely pigmented hairs develop within 3 to 4 months if treatment is successful.

3. Systemic (oral or IV) corticosteroids can be considered. However, they should not be used for long periods of time due to risk of side effects.

4. Contact sensitizers such as squaric acid dibutylester or diphencyprone

a. Patients are first sensitized to the agent with a 2% concentration in acetone.

b. After 1 week, a 0.001% solution is applied to all affected areas on one side of the scalp. This is repeated weekly.


c. Concentration is titrated up according to previous weeks reaction. Goal reaction is to maintain lowgrade erythema, with or without scaling and pruritus, for 2 to 3 days after application.

d. Regrowth consisting of white or finely pigmented hairs develop within 3 to 4 months, if successful.

e. If no growth in 3 to 4 months, consider another therapy.

5. Topical anthralin

a. Apply lowest concentration to affected area daily.

b. If no hair growth, concentration may be increased to 1.0%. Apply to affected area 20 to 30 minutes daily.

6. Topical minoxidil

a. Positive results seen in only a small percentage of patients.

b. May take up to 4 months to see regrowth.

c. Will keep working only as long as used.

d. New hair may be lost when drug is discontinued.

7. Other topical irritants, such as tazarotene or azelaic acid, may be of limited benefit.

8. Light therapy

a. Psoralens, topical or systemic, with ultraviolet

A. Successful in only a small percentage of patients.

b. Excimer laser—focal narrow band UVB.

c. Photodynamic therapy.

9. Other compounds with limited studies, but some reported benefit, include isoprinosine, total glucosides of paeony capsules, topical garlic gel (in combination with topical steroids), and aromatherapy.

10. Oral antidepressants.

B. Surgical interventions: none



ANDROGENIC ALOPECIA


I. OVERVIEW

A. Definition: androgenic alopecia is the most common cause of thinning hair. There are two types, male pattern (common baldness) and female pattern hair loss.

B. Etiology

1. Inherited condition from either parent

C. Pathophysiology

1. Regression depends on androgen production with normal serum androgen levels found.

2. Process is progressive beginning with hair shedding, followed by smaller hair shaft diameter “miniaturization,” shortening of anagen, and lengthening of telogen growth phases.

3. Total number of hair follicles nearly normal (about 35 per 4-mm plug).








TABLE 22-1 Classification of Male Androgenic Alopecia











































Type


Clinical Features


I


Normal frontotemporal hairline.


II


Symmetric triangular areas of recession in the frontoparietal regions. Hair also lost along midfrontal scalp border.


II-Aa


Anterior hairline high on forehead.


III


Deep frontotemporal recession. Minimal extent of hair loss considered to represent baldness. Vertex type—hair is lost chiefly at the vertex with or without frontal recession.


III-Aa


Alopecic area extends to middle crown area.


IV


Deep frontal and frontotemporal recession in association with hair loss at the vertex.


IV-Aa


Alopecia extends past midcrown of scalp with posterior thinning.


V


The separation from recessed frontal and frontoparietal alopecia to the vertex area of alopecia now narrower and more sparse than in type IV.


V-Aa


Area of alopecia not entirely to vertex. Most advanced stage of type A variant.


VI


Frontotemporal and vertex areas of alopecia now confluent. Area of alopecia has extended laterally and posteriorly.


VII


Most severe male pattern baldness with only a narrow horseshoe-shaped band of hair remaining.


a Type A variant: Major criteria must be present: anterior hairline recedes posteriorly with no midfrontal island of hair; no concomitant thinning at the vertex. Minor criteria common but not necessary: sparse hairs persist in alopecic area; wreath of remaining temporal and occipital hair wider and higher than in non-A variant.


Adapted from Norwood, O. T. (1975). Male pattern baldness: Classification and incidence. Southern Medical Journal, 68(11), 1359-1365.


4. Reduced number of terminal hairs.

5. Increased number of vellus hairs.

6. Increased telogen count when compared with uninvolved scalp.

D. Clinical features

1. Occurs most commonly in late adolescence or in early 20s.

2. Patterns of male androgenic alopecia (Table 22-1, Figure 22-4).

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Mar 9, 2021 | Posted by in NURSING | Comments Off on Hair and Nails
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