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Musculoskeletal/Skin > 3/4 - Adnexal Structures/Disorders and Melanocytes/Disorders > Flashcards

3/4 - Adnexal Structures/Disorders and Melanocytes/Disorders Flashcards

1
Q

What are the components of the pilosebaceous unit?

A

Infundibulum

Isthmus (makes hair stand up)

Inferior segment: containing the bulb and the matrix

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2
Q

In which part of the pilosebaceous unit are mitotically active undifferentiated cells present?

A

The hair bulb!

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3
Q

What are the three types of hair in the pilosebaceous unit?

A
  1. Lanugo (fetal): seen on babies
  2. Vellus (fine) fine hairs often seen on the legs or arms of young children
  3. Terminal (coarse) seen on beard, axilla, or pubic hair
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4
Q

What are examples of conditions in which you would see abnormal hair types for age or location?

A

Anorexia (lanugo): hair in places you wouldnt normally have hair

Hirsutism (terminal): females with erminal hairs in male pattern distribution may indicate androgen excess/polycystic ovarian syndrome

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5
Q

What are sebaceous glands? How do they work and when are they active?

A

Glands with the greatest density on the face and scalp (but are everywhere).

Produce sebum (oil) via holocrine secretion: triglycerides, free FAs, squalene, wax and sterol esters, and free sterols.

Active at birth but decrease during infancy. Sebum production stimulated by androgran produciton (5-alpha dihydrotestosterone) in puberty.

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6
Q

Name each structure in blue

A
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7
Q

What is occuring in this image?

A

Cells of the sebaceous gland have lipid packages that break down.

The sebocytes lose their nucleus as they move through the gland to be secreted as oil.

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8
Q

What are the phases of the hair cycle? How long does each phase usually last?

A
  1. Growth phase - Anagen: majority of hair in the scalp is in anagen and duration dictates hair length. 85% of hair is in thie stage and it lasts 2-5 years.
  2. Transition phase - Catagen: growth stops, lasts for weeks to months. Lasts 3-6 weeks.
  3. Resting phase - Telogen: hair is shed during this phase. Up to 15% of hair is in this phase; can last 3-5 months.
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9
Q

What is telogen effluvium? What can cause this?

A

A hair cycle disoder: greater proportion of hair is in the telogen (resting) phase of the cycle where the hair is shed.

Patients report increase in hair shedding. Secondary changes not common, NO discrete patches of alopecia.

Usually occurs ~3mo after a stressful event and slowly returns to normal.

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10
Q

What is alopecia areata? How is it treated?

A

An autoimmune disoder characterized by patches of hair loss that are variable in size and tend to be focal. Nail pits (indentations in the nail plate) may occur.

Secondary changes not common (erythema, scale) not common.

Topical corticosteroids are the mainstay of treatment.

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11
Q

What are the two types of sweat glands? How do they differ?

A

Eccrine (sweaty): on palms and soles; innervated by sympathetic fibers via acetylcholine. Go directly to skin surface.

Apocrine (sweaty and smelly): axillae, anogenital, periumbilical, areolae, and vermillion border of the lips. Pretty big; attach to hair shaft.

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12
Q

What are two examples of disorders of sweat glands?

A

Hyperhidrosis: overactivity of sweat glands

Anhidrosis/hypohodrosis: occurs when sweatglands are absent/reduced (eg ectodermal dysplasia)

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13
Q

What are three disorders of the pilosebaceous unit?

A
  1. Acne vulgaris
  2. Acne rosacea
  3. Tinea versicolor
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14
Q

What is acne vulgaris caused by?

A

When sebaceous cells (via sebum or fatty acids) or follicular keratinocytes ( via hyperprolif, increased keratohyalin granules, or disturbed dequamation) get clogged (microcomedo)

These factors can all be increased by androgens such as DHT and testosterone.

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15
Q

What types of acne caused by microcomedo?

A

Closed comedo: white heads

Open comedo: black heads due to oxidation of material

Inflammatory lesions: from P acnes.

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16
Q

What is the pathogenesis of acne?

A

Propionibacterium acnes: gram positive rod that’s dependent on glycerol and causes the hydrolysis of sebum triglycerides.

Produces: porphyrins, proinflammatory mediators, and lipases.

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17
Q

What is the function of retinoids?

A

Treats P ances and follicular keratinocytes that cause microcomedo.

Causes faster shedding of the cornified layer.

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18
Q

What is the funciton of antibiotics on acne?

A

Can be used topically and orally for anti-inflammation.

Treats P acnes and follicular keratinocyte microcomedo.

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19
Q

What are three systemic treatments for acne?

A
  1. Antibiotics
  2. ORal contraceptives
  3. Isotetinoin
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20
Q

What antibiotics can be used to treat acne?

A

First line: tetracyclines such as doxycycline and minocycline that work to inhibit P. acnes and decrease inflamamtion (by reducing proinflammatory mediators).

Others: erythromycin, bactrim, penicillins

21
Q

What are the side effects of doxycycline and minocycline for treatment of acne?

A

Doxycycline: pill esophagitis, photosensitivity

Minocycline: drug hypersensitivity syndrome, drug-induced lupus, hepatitis

22
Q

How can oral contraceptives treat acne? What types of acne can they treat? What are side effects?

A

Blocks production of androgens (adrenal and ovarian) and increase sex-hormone binding glubulin to decrease free testosterone.

Treats inflammatory papules/pustules and peri-menstrual flares.

Side effects: nausea, vomiting, abnormal menses, weight gain, breast tenderness, thrombophlebitis, and HTN.

23
Q

When is isotetinoin indicated to treat acne? How does it work?

A

Systemic retinoid with anti-inflammatory properties.

Indicated for severe nodulocystic acne, scarring, or severe acne recalcitrant to systemic antibiotic therapy and topicals.

Cumulative dose: 120-1590 mg/kg; achieved by 1mg/kg/day divided BID x 5mo

24
Q

What is tinea versicolor? What are the primary lesions and secondary changes?

A

Malassezia spp (globosa and furfur) fungus that causes oval to round scaly patches with fine overlying scale.

Primary lesions: macules, patches

Secondary changes: color (hypo or hyperpigmentation), scale

25
Q

What are the primary lesions of acne vulgaris?

A

Papules (including comedones), pustules, nodules, and cysts.

26
Q

What are melanocytes and what surrounds them?

A

Cells derived from neural crest that live on the basal layer of the epidermis and produce pigment.

Dendrites extend to multiple keratinocytes to facilitate melanin transfer.

Epidermal-melanin unit is the melanocyte and its surrounding keratinocytes (roughly 1:10 ratio).

27
Q

Where can melanocytes be found?

A

Hair, skin, retina, iris, inner ear, and medulla oblongata.

28
Q

What is stained brown here?

A

Melanocytes and nearby melanosomes (brown spots), which are the pigment granules in keratinocytes.

29
Q

What determines skin pigmentation?

A

The size, number, and density of melanosomes (pigment granules in keratinocytes)

Menanocyte number and density does NOT vary by race.

30
Q

Describe the formation of a melanosome?

A

Modified in golgi and forms endosome that starts to accumulate pigment.

Tyrosinase forms melanin - defects can cause things like albinism

31
Q

What can you determine about the individuals skin tone (left) based on these pictures?

A

The abundance of melanin in the basal cell layer indicates that the individual on the left has a darker skin tone that the person on the right.

32
Q

What are the different type of pigmentation that can occur? How can you tell the difference?

A

Hyperpigmentation: darker than surrounding or normal color; increased pigment

Hypopigmentation: lighter than surrounding skin; decresed pigment

Depigmentation: white; not pigment

Can use a woods light to help differntiate “white” areas frmo “light” areas.

33
Q

What disease is indicated by the presence of 3 or more ash leaf macules (pictured)? How common is this and what is the underlying genetic problem?

A

Tuberous Sclerosis: autosomal dominant genetic disorder that causes non-malignant tumors of the brain, eyes, heart, kidneym skin, and lungs.

1/5800-10,000 births

TSC1 (hamartin), TSC2 (tuberin) mutations, 2/3 of which are new/spontaneous mutations

34
Q

Other than ash-leaf macules, what other clinical findings are consistent with tuberous sclerosis?

A

Angiofibromas: apepar later; thickened collagen across nose and inner cheek

Fibrous plaques: around hairline; collection of angiofibromas

Shagreen patches: less common but may occur; connective tissue growth (collagen) usually on trunk.

Periungal fibromas: similar to what happens on face

35
Q

What is Vitiligo?

A

T cell mediated autoimmune disorder involving the destruction of melanocytes with subsequent development of depigmented patches.

Typically acquired (not present at birth) and progressive.

Hair in affected areas often becomes white (poliosis).

36
Q

What is oculocutaneous albinism? What are characteristics?

A

Genetic disorder (autosomal dominant or recessive) caused by a defect in tyrosinase or related proteins resulting in impaired or limited melanin production.

White to yellow/red hair with light to yellow skin depending on the type of albinism.

37
Q

What are the different types of brown spots?

A
  • Ephelides: freckles
  • Café au lait macules
  • Solar lentigo/lentigines
  • Dermal melanocyttosis
  • Melanocytic nevi (acquired)
  • Congenital melanocytic nevi
38
Q

What are these called?

A

Café au lait macules

39
Q

What is neurofibromatosis 1 (NF1) caused by? How common is it?

A

Von Recklinghausen’s disease. Autosomal dominant disease caused by mutations in neurofibromin.

Up to 50% spontaneous mutations.

Birth incidence 1/3000

40
Q

What are clinical manifestations of neurofibromatosis 1 (NF1)?

A
  • Café au lait pigmentation (more than 5)
  • Axillary/inguinal freckling (mini café au laits)
  • Neurofibromas (little growths that are soft and may or may not hurt)
  • Plexiform neurofibromas (can interefere with life, be painful/disfiguring)
41
Q

What is solar lentigo?

A

“age spots” “liver spots”

Occur on sun-exposed areas; bigger than ephelids.

42
Q

What is dermal melanocytosis? Where does this occur?

A

“mongolian spots”

Deeper pigment (in lower dermis) that creates a blueish color.

Lumbosacral location is the most common; usually fade over time

43
Q

What are the different types of melanocytic nevi?

A

Acquired; subtypes have more histologic significant than clinical and refer to location of melanocytic nests.

  • Compound
  • Junctional
  • Intradermal
44
Q

How do you determine the danger of melanocytic nevi?

A

Risk of malignant transformation to melanoma; self skin exam is crucial to early detection.

A: asymmetry

B: border irregularity/blurred border

C: Color heterogeneity

D: Diameter >6mm (not applicable to congenital lesions)

E: evolution or change

45
Q

What are the different types of congenital melanocytic nevus (CMN)? What is the risk involved in having these?

A

Small, medium, and large (giant).

Large (giant) CMNs have a higher risk for melanoma than small CMN. Pts with these also at risk for neurocutaneous melanosus - leptomeningeal melanosis or even melanoma (malenocytes in the meninges and brain interefere with brain development).

46
Q

What are some causes of brown spots that occur early in life?

A
  1. Ephelides: freckles
  2. Neurofibromatosis (6 or more cafe au lait macules)
  3. Congenital melanocytic nevi
47
Q

What are some causes of brown spots later in life?

A
  • Melanocytic nevi
  • Solar lentigo
48
Q

What are some causes of white spots early in life?

A
  • Tuberous sclerosis (3 or more ash leaf macules)
  • Oculocutaneous albinism
49
Q

What is a cause of white spots later in life?

A

Vitiligo

Musculoskeletal/Skin (29 decks)

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