Hair Nails and Oral Mucosae Flashcards

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1
Q

What is a hair follicle, where is it NOT located.

A

* elongated keratinized structure derived from invaginations of epidermal epithelium.

* Not located at: palms, soles, lips, glans penis, clitoris, labia minora

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2
Q

Define infundibulum, isthmus, lower portion of hair folicle.

A

Indundibulum: opening of hair follicle to opening of sebaceous duct.

Isthmus: from sebaceous duct opening to insertion of arrector pili muscle. (contraction arrector pili = goosebumps).

Lower portion: formed by hair bulb which is composed of papilla (contains inductive firbroblasts for prolif/differentiation) and matrix (melanocytes for hair color).

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3
Q

What are the sections of the hair shaft?

A

medulla: central portion. Consists of spongy keratin with air spaces of variable sizes. Only found in terminal hair.

Cortex: Condensed macrofibrils/melanin. Forms main bulk of hair and contributes to the mechanical properties of hair.

Cuticle: 6-8 layers of cuticle cells, overlapping like roof tiles, free margin always pointing upward.

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4
Q

Inner vs outer root sheaths of hair follicle.

A

Inner root sheath: Rigid cylindrical tube, develops before the hair within it and its prime function is to mould the hair. It disintegrates at the level of the sebaceous gland.

Outer root sheath: derived from/continuous with epidermis. Function unknown. Surrounded by glassy BM which is in turn surrounded by CT sheath which has important inductive properties.

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5
Q

Describe the chemical composition of hair

A

Main component = protein (65-95%), lots of S-S bonds. Very hygroscopic (wet hair is easier to break).

Lipids: useful as water repellent, increases at puberty then declines with age.

Trace elements: Cu, Cd, Cr, Pb (come from exogenous sources such as cosmetics, air pollution) or from endogenous sources (matrix, papilla, sebaceous/sweat glands)

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6
Q

What are the 3 phases of the hair growth cycle

A

Anagen: active growth phase. 1000 days for the scalp, 28 days for eyebrows. ~85-90% of hair in anagen.

Catagen: phase of involution. Completion in a few days.

Telogen: resting phase. Clubbed hair duration = 100 days.

E.g. ratio of anagen/telogen on scalp 9:1, eyebrow 1:9

(shaving has no impact on rate of hair growth)

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7
Q

How does cross-sectional shape affect hair texture?

A

Round x-section: straight hair (e.g. Asian) Oval x-section: wavy (e.g. white) Flat x-section: curly/kinky (e.g. black)

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8
Q

Name the non-scarring alopecias (7)

A
  1. Androgenic alopecia
  2. Alopecia areata
  3. Trichotillomania
  4. Tinea capitis
  5. Telogen capitis
  6. Telogen effluvium
  7. Anagen effluvium
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9
Q

Describe androgenic alopecia

A

50% of men and women experience by 50 yrs

Each individual follicle is genetically marked to become bald or no.

Uptake, metabolism and 5-alpha reduction of testosterone is increased in balding areas.

Can be maternally or paternally inherited.

Treatment: oral finasteride, topical minoxidil, hair transplant sx

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10
Q

What is alopecia areata

A

Autoimmune disease causing circumscribed circular patch or patches of hair on scalp.

Includes exclamation point hairs (!) which taper proximally and are pathognomonic

In periphery: may have short, broken hairs

Asymptomatic but may be paraesthesias or tenderness.

Can affect eyebrows and beard.

Course is unpredictable but early age of onset and atopy (hyperallergy) indicates a lengthier course and increased incidence of alopecia totalis (totally bald)

50% of cases resolve in 1 yr without treatment (note that initially returning hair may be de-pigmented). 25% have famHx.

Tx options: corticosteroid injections at localized patches. For totalis: immunomodulators (e.g. ?DCPC or ?SADB)

Associations: 8% thyroid disease, 4% vitiligo. Nail changes such as pitting occur in up to 40% of cases.

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11
Q

Describe trichotillomania

A

Repetitive hair pulling or plucking resulting in patchy, unnatural pattern.

Peripheral portions of scalp usually spared.

Less than 5% have deep seated psychological disorders.

May be LIFE THREATENING if there is concomitant trchophagy (swallowing of hair). Trichobezoards can cause partial obstruction of the intestine.

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12
Q

Describe tinea capitus

A

Most common cause = Microsporum canis, found on cats and dogs. Not contagious from human to human.

Trichophyton tonsurans: 2nd most common organism. Contagious human-human. Cases may be inflammatory or non-inflammatory. Inflammatory causes may become secondarily infected with staph and scarring can occur.

Diagnosis: KOH scraping, mycologic culture, Wood’s lamp (only hairs infected wby microsporun species will fluoresce due to pteridine substance it produces)

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13
Q

Describe telogen effluvium

A

Excessive shedding of normal club hairs can be brought about by a number of stressors: fever, stress, diets, drugs (beta blockers, anticoagulants, anti-thyroid)

Stress factors cause termination of anagen and progression to catagen then TELOGEN.

In 2-4 months telogen hairs are pushed out. 50K new hairs must be lost before visible thinning. Scalp normally has 100K. Normal regrowth in 6 months.

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14
Q

Describe anagen effluvium

A

Pathologic loss of anagen growth phase with decrease or complete discontinuance of proliferation of matrix cells of hair shaft. Occurs after a few days to weeks after insult

Potential insults: chemo, radiation

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15
Q

Describe scarring (cicatricial) alopecia

A

Far less common than non-scarring alopecias. Important to recognize because of potential for irreversible permanent hair loss. Can be caused by discoid lupus erythematosus or lichen planopilaris.

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16
Q

What is a nail?

What is the function of a nail?

A

Nails are plates of keratinized epithelial cells on the dorsal surface of each distal phalanx.

Functions:

  1. Protect distal phalanx from trauma
  2. Help picking up objects
  3. Aid in appreciation of fine touch
  4. Scratching
  5. Aesthetics
  6. Animals: locomotion or as a prehensile organ
17
Q

What are the components of a human nail?

A
  1. Nail plate: horney end product of the nail matrix. Is 0.5 mm thick, covers fingertip. Corneocytes are flattned, anuclear and devoid of organelles. Composition: hard keratin with high sulfur content = main component. High glycine-Y rich matrix protein. 18% water, lipid <5%. Rigidity depends on arrangement of cells, their adhesions and the orientation of keratin fibers.

Nail unit:

  1. Nail fold/Lovibond’s angle: angle between the nail plate and dorsum of the digit skin. Proximal nail fold is an extension of the dorsal skin of the digits as a fold lying superficial to the matrix. Is the site where abnormal capillary patterns can be visualized in certain diseases (SLE, systemic sclerosis). Cuticle is the extension of horny layer of eponychium into the dorsum of the nail plate and serves to protect the structures at the base of the nail.
  2. Matrix: melanocytes may be present contributing to pigmentation fo the nail plate. Lunula = most distal part of matrix.
  3. Nail bed: pink in colour due to enriched vascular network. Epidermis is very thin, horny layer scant, granular layer absent.
18
Q

Describe nail growth and development.

A

0.5-1.2 mm/week

The longer the finger, the more rapid the growth.

Toenails grow at 33-50% the rate of fingernails.

Regeneration of a fingernail after avulsion is 160 days (40 days to emerge from nail fold, 120 for growth to fingertip)

19
Q

Describe nail dystrophy

A

Damage to the nail as a result of trauma or disease results in dystrophy, this is the presence of a misshapen or partially destroyed nail plate, resulting elevation of the plate.

20
Q

What is onychomycosis?

A

Fungal infection is an extremely common cause of toenail dystrophy.

Great toenail is extremely prone to infection.

Infection of fingernails occurs only in nails previously traumatized or when nail involvement is part of tinea mannum.

  • *Onycholysis**: separation of nail plate from nail bed
  • *Subungual hyperkeratosis**: buildup of soft yellow keratin in the space created by the onycholysis, usually asymptomatic
  • most due to Trichophyton rubrum, but in a few cases, Epidermyophyton floccosum and Trichophyton mentagrophytes may be recovered. Diagnosis can be made by culture.

Treatment: terbenafine or itraconazole orally.

21
Q

Describe psoriasis of the nail.

A
  • onycholysis, subungual hyperkeratosis, nail pitting, yellowish discoloration
  • more serious nail dystrophies are often accompanied by inflammatory, arthritic changes in the distal interphalangeal joint
  • extremely difficult to treat
22
Q

What are Beau’s Grooves of the nail?

A

1 mm wide depressions in the nail plate which extend horizontally from one lateral nail groove to the other

All nails are simultaneously affected

Most commonly develop following dramatic illness such as MI and periods of high fever or malnutrition

23
Q

Describe nail clubbing.

A

Lovibond’s angle greater than 180 degrees, most commonly seen with chronic pulmonary or cardiopulmonary disease but also occurs with some tumors, especially those of the lung parenchyma

24
Q

Describe periungual warts.

A

Often distort the nail plate

In most instances, the dystrophy is not permanent and the nail plate returns to normal following therapeutic or spontaneous resolution of the warts

25
Q

What is white banding of the nail?

A

Horizontal white banding or opacification occurs in hypoalbuminemia accompanying chronic hepatic or renal disease.

26
Q

What is brown banding of the nail?

A

Vertical: secondary to nevus or melanoma

Horizontal: Addisons disease or cancer chemotherapy

27
Q

What are spinter hemorrhages of the nail?

A

Thin, dark red lines, 1-3 mm in length
.

Represent small hemorrhages at the junction of the nail plate and the nail bed.

Move out as the nail grows.

May indicate: bacterial endocarditis, trichinosis, frequent in normal individuals.

28
Q

Describe Candida Paronychia

A

Inflammation of the nail folds caused by Candida. Most common cause of paronychial inflammation and swelling of the fingers.

Paronychia: inflammation or swelling at base of nail or surrounding skin.

Seen in dishwashers, bartenders, waitresses

Characterized by: lack of pain, lack of warmth. Absence of pus. Chronicity.

29
Q

Describe Bacterial Paronychia

A

Usually due to staph infection.

Causes redness, warmth, swelling and tenderness.

30
Q

What is the differential for white lesions of the mouth?

A
  1. Lichen planus
  2. Candida
  3. Verrucae (wart)
  4. Squamous cell carcinoma
  5. Lupus erythematosus
  6. Syphilis
  7. Oral hairy leukoplakia
31
Q

What is the differential for ulcerating lesions of the mouth?

A
  1. Herpes simplex – small grouped blisters first presentation
  2. Aphthous stomatitis: punched out ulcers – not caused by herpes simplex virus (benign, non-contagious often recurrent. Typical oral ucler)
  3. Behcet’s syndrome: rare disorder causing inflammation of the blood vessels.
  4. Lichen planus
  5. Pemphigus/pemphigoid: skin disease with watery blisters
  6. Stevens Johnson syndrome/erythema multiforme major
32
Q

Describe the anatomy of the oral mucous membranes.

A

Lips: vividly pinkish-red (vermilion) surround entrance to oral cavity
Vermillion Border: between oral mucosa and skin. No evidence of keratinization.
Labial mucosa: mucous saliva can be detected as secretions from numerous orifices of the minor salivary glands. Maxillary and mandibular labial mucosa are attached to gingiva and alveolar bone by a midline frenum.
Buccal mucosa: minor salivary glands.

Linea alba: white ridge where the teeth rest.

Fordyce granules in 75% of individuals. They are ectopic sebaceous glands and present as <2mm yellow papules.

Tongue: muscle covered by keratinized mucosa containing taste buds. Accessory lymphoid tissue or lingual tonsil is normally found in healthy individuals. Sublingual veins are present on the undersurface of the tongue. The lingual frenulum originates in the midline of the ventral tongue and inserts into the floor of the mouth.

Hard Palate: covered by parakeratinized epithelium. Appears as a lighter pink due to keratin and a less vascular lamina propria.

Soft palate: lacks osseous support, is highly mobile and extends posteriorly closing the nasopharynx. Uvula is a midline extension of the soft palate.

33
Q

What is the difference between exogenous and endogenous pigmentation of the oral mucosa?

A

Exogenous materals that can hyperpigment the oral mucosa:

Foreign materials: amalgam tatoos, carbon, seeds, leaves of various plants, tobacco Pharmacologic agents: minocycline, AZT, antimalarials, amiodarone, OCP, doxorubicin
Heavy metal exposure: bismuth, mercury silver, lead, tin, copper

Endogenous factors that can hyperpigment the oral mucosa:

Systemic disease: Addison’s disease. Peutz-Jeghers syndrome, hemochromatosis

Neoplasms: nevi, oral and labial melanotic macules, melanoma

Reactive process: postinflammatory hyperpigmentation