Adnexal Structures and Associated Disorders

Question 1

Lanugo hair

Answer 1

Fetal hair follices

Question 2

Vellus hair

Answer 2

Very fine hair

Question 3

Terminal hair

Answer 3

Coarse, darker hair. Adult hair. Usually apparent by puberty, but androgens may convert vellus hair to terminal (beard, axillae, pubic)

Question 4

Pilosebaceous unit

Answer 4

Consists of hair follicle and its associated sebaceous gland

Question 5

Holocrine secretion

Answer 5

Sebocytes in sebaceous glands disintegrate and relase their sebum as they migrate toward the duct. Continuous but variable flow

Question 6

Areas with sebacious glands without accompanied hair

Answer 6

Nipples, eyelids, orogenital tract

Question 7

Anagen phase

Answer 7

Growth phase of hair. 2-6 year period. 85% of hair follicles on scalp.

Question 8

Catagen phase

Answer 8

Regressive phase. 2-3 weeks. 1% of scalp or less

Question 9

Telogen phase

Answer 9

Resting phase. 3 months. 10-15% of scalp

Question 10

Growth phase variation?

Answer 10

Longer growth phase periods results in longer hair. Scalp has the longest anagen phase, explaining why hair on the scalp can grow so long.

Question 11

Telogen effluvium

Answer 11

Greater proportion of hair follicles enter telogen phase simultaneously due to STRESS

Pregnancy, fever, surgery, illness, malnutrition

3 months post-stress, we will see the hair loss. This is because telogen phase on the scalp is 3 months long.

Question 12

Alopecia areata

Answer 12

Autoimmune.
Sudden development or round of smooth patches of hair loss (alopecia)

Can progress to alopecia totalis or alopecia universals

No erythema, scaling, or pustules. Helps to distinguish it from tinea capitis.

Treat with corticosteroids

Question 13

Anagen effluvium

Answer 13

Chemo/drug induced hair loss.

2-3 weeks post-drug administration

Question 14

Eccrine glands

Answer 14

Greatest density in palms and soles. Active from birth, unlike sebacious glands (Which taper after parting from mother).

Innervated by postganglionic sympathetic fibers from hypothalamic sweat center. Acetylcholine stimulated.

Each unit has: Coiled secretory portion in lower dermi and thin duct apically (acrosyringum) that opens to skin surface. Only referred to as acrosyringum while in the epidermis portion.

Two cell times in the secretory coil: Large clear cells that release gland’s electrolytes and water and dark cells that produce sialoucin.

Myoepithelial cells surround the secretory coil to enhance delivery

Duct is made of 2 cuboidal epithelium cells

Question 15

Eccrine gland sweat product

Answer 15

Isotonic at release, but readsorption of NaCl by duct cells makes it hypotonic at surface.

Question 16

Eccrine gland function

Answer 16

1) Thermoregulation by evaporative heat loss
2) Electrolytic balance.
3) Maintenance of moist stratum corenum to facilitate tactile skills, pliability of the palms and soles.

Question 17

Apocrine glands

Answer 17

Unclear function. Their product is oily and odoriferous. Enlarged during puberty. High density in axillae, anogenital region, etc.

Modified versions: Auditroy canal and eyelid margin (ceruminous glands and glands of moll)

Single columnar epithelial secretary center, with myoepithelial cells surrounding. Plus a double cuboidal duct.

Question 18

Acne Vulgaris

Answer 18

Initially due to sebum production rise in response to hormones, along with impaired corneocyte shedding

This results in a hair follicle plug (comedo formation)

Plugged follicles can rupture, causing inflammation in response to the extruded keratin and sebum

Propionibacterium acnes is a gram pos non-motile rod in the follicle that plays a role, too.It does this by promoting follicular rupture, and stimulates neutrophil recruitment and Th1

Question 19

How does adrenarche contribute to acne?

Answer 19

Rising levels of DHEAS as adrenal gland picks up, that is converted into more potent androgens in the sebaceous gland. Results in more sebum production

Question 20

Main things in non-inflammatory acne?

Answer 20

Comedones. Closed comedones are white heads, while open comedones are blackheads. Can have scarring, but rare.

Question 21

Main things in inflammatory acne?

Answer 21

Pustules (neutrophil response) or inflammatory papules/nodules/cysts( mixed response that includes lymphocytes, giant cells and neutrophils) occur. Scarring more common. Hyperpigmentation can occur, but will go away after several months.

Question 22

How do retinoids target comedones?

Answer 22

Normalize follicular keratinization, expel existing keratinaceous follicular plugs and prevent new lesions from forming

Bind RAR and RXR intracellularly, which heterodimerize and modifying transcription.

Question 23

Antiinflammatories for acne?

Answer 23

Benzoyl peroxide, clindamycin and erythromycin

Also function as P. acnes antibiotics.

Orally active drugs include doxycycline and minocycline

Question 24

Acne rosacea

Answer 24

Blushing, reddened complexion due to vascular hyperreactivity

May have papules, pustules, telangiectasia

Overgrowth of sebacious glands, making skin look swollen

No comedones!

Treat with metronidazole or sodium sulfacetamide, but these patients can have their skin easily irritated and have to stop treatment

Question 25

Melanocytes

Answer 25

1. Derived from neural crest 2. Basal layer of epidermis. 3. Release melanin Ratio of melanocytes to keratinocytes is 1:10

Question 26

Vitiligo

Answer 26

Depigmented patches Symmetric involvement Facial (especially perioral) involvement common Unpredictable course, and can resolve Treat with corticosteroids Last line therapy is UV phototherapy to stimulate repigmintation

Question 27

Albinism

Answer 27

Defect in melanin production (cutaneous or oculocutaneous) Decreased visual acuity and nystagmus common High skin cancer risk

Question 28

Piebaldism

Answer 28

``` Autosomal dominant White patches (poliosis), and skin SEctions of skin or hair lacking melanocytes Stable condition that does not progress. ```

Question 29

Waardenburg Syndrome

Answer 29

``` Autosomal recessive Achromic (white) hair, skin or both Medial eyebrow hyperplasia (unibrow) Heterochromia irides (eyes two colors) Broad nasal root Dystopia canthorum (widened inner eye distance) ```

Question 30

Melanocytic nevi

Answer 30

Benign melanocytic proliferation Starts junctional (at epidermal/dermal boundary), then becomes compound (in both the junction and in the dermis), and finally ages to intradermal where it is totally confined to the dermis

Question 31

Congenital melanocytic nevi

Answer 31

Very large compaired to acquired melanocytic nevi Can be 1 cm to 20 cm, found at birth If large, can be a risk for melanoma ABCDE A = Asymmetric B = Border irregular or blurred C = Color heterogeneity D = Diameter of 6 cm (not applicable if congenital) E = Evolution or changing morphology and size

Question 32

Ephelides

Answer 32

Freckles. Occur on sun-exposed portions of the body. A sign of UV-induced damage. Increased melanoma risk

Question 33

Cafe-au-lait spots.

Answer 33

Congenital or from infancy. Well-circumscribed. Fine to have a couple, but if many are present it can be a sign for neurofibromatosis

Question 34

Solar lentigo

Answer 34

Dark brown or black macules due to UV light. Later in life, larger (5-15 mm in size) Chronic sun exposure.

Question 35

Dermal melanocytosis

Answer 35

bluish-gray infantile patches in the lumbrosacral region in Asians more commonly Secondary to melanocytes in the middle to lower dermis (deeper than brown lesions) Very large

Question 36

Acanthosis nigricans

Answer 36

Due to diabete; manifestation of insulin resistance (type II) Also associated with familial syndromes and cancer Brown, velvety plaques in posterior neck, axillae and groin (form in the creases)

Question 37

Diabetic dermopathy

Answer 37

A marker for poor diabetes control. Brown, atrophic macules on the shins. Trauma may set them off.

Question 38

Necrobiosis lipoidica diabeticorum

Answer 38

Shins of diabetic patients Yellow orange atrophic patches Expand into ulcerations No association with diabetic control

Question 39

Diabetic Bullae

Answer 39

Arise spontaneously on extremities. Self resolve but can recur. More common in men with long standing disease or complications

Question 40

Hyperthyroid derm effects

Answer 40

Pretibial myxedema on the shins, due to deposition of Hyaluronic acid on skin... Lesions that are bilateral, firm, nonpitting, shiny and pink Also have velvety, smooth skin that is moist and sweat more. May lose hair diffusely

Question 41

Hypothyroidism derm effects

Answer 41

Dry, rough skin Loss of lateral third of eyebrow hair

Question 42

Cushing's derm effect

Answer 42

Striae, cutaneous fragility, purpora from minor trauma Full chese, rounded faces, fat pads on upper back Loss of arm and leg fat (lipodystrophic) More cutaneous infection

Question 43

Addison's disease derm effects

Answer 43

Hyperpigmentation, especially gingiva and mucous membranes and skin creases (axillae, groin, palms)

Question 44

Prophyria cutanea tarda

Answer 44

Defect in uroporphyrinogen III decarboxylase (UROD). Usually due to liver disease. Sometimes due to autosomal dominant mutation Adult onset. Vesicles on skin that heal with scarring when exposed to sun Face and hands Treat with iron chelation therapy

Question 45

Lupus flares

Answer 45

Usually photosensitive. Lupus in general more common in females

Question 46

Systemic Lupus erthematosus

Answer 46

Multisystem form. Malar/butterfly rash Accompanied by alopecia, oral ulcers, raynaud phenomenon

Question 47

Discoid lupus erythematosus

Answer 47

Minority of SLE patients. Skin limited (not multiorgan) Hyperkeratotic, violaceous plaques Head and neck, scalp and ears Atrophic scarring

Question 48

Subacute cutaneous lupus erythematous

Answer 48

Skin-limited, associated with internal disease sometimes Pink scales on sun-exposed skin

Question 49

How to treat lupus?

Answer 49

Corticosteroids

Question 50

Dermatomyositis

Answer 50

Female predominant autoimmune disease Heliotrope rash, pink-purplse discoloration of upper eyelid. Eyelid can also be edematous. May have scaly pink patches in scalp, malar region... Also can have shawl sign scales (chest/shoulders/back) Gottron's papules (pink/purple papules on elbows, knees, dorsal hands)

Question 51

Sarcoidosis

Answer 51

Most common in African American men Pleomorphic Noncaseating granulomas in multiple organ systems Must be tested for organ involvement, since it can be asymptomatic Red-brown macules and papules on face around eye and nose

Question 52

Dermatitis Herpetiformis

Answer 52

Autoimmune blistering disease Gluten hypersensitivity Common in men, young adults Pruritis, the vescicles will be eroded and excoriated at exam Treat with dapsone and gluten free diet

Question 53

Neurofibromatosis Type I

Answer 53

NF-1 gene mutation in neurofibromin. Autosomal dominant Cafe-au-lait macules Axillary and inguinal freckling (regions that don't get sun) Neurofibroms develop (rubbery papules) Plexiform neurofibromas also develop (very large plaques, feel like a bag of worms)

Question 54

Tuberous Sclerosis

Answer 54

Autosomal dominant Benign angiofibromas on the face Mutations in TSC1 and TSC2 (hamartin and tuberin) Periungual fibromas in nails Hypomelanotic macules and patches Shagreen patches (leathery plaques on lower back)

Question 55

Sturge-Weber Syndrome

Answer 55

Port wine stain (capillary malformation) present at birth on opthalmic trigeminal distribution Cerebral calcifcation and seizure Glaucoma ipsilaterally

Question 56

PHACE syndrome

Answer 56

``` Posterior fossa brain malformation Hemangiomas on face Arterial cerebrovascular anomalies Cardiovascular anomalies Eye anomalies ```

Question 57

Topical corticosteroids

Answer 57

All from glucorticoid family. Anti-inflammatory

Question 58

Steroid side effects

Answer 58

Reversible: hypopigmentation, hypertrichosis, skin atrophy, telangiectasia Irreversible: Striae Allergies also possible

Question 59

Ointments

Answer 59

Pros: occlusive barrier, better penetration and moisturizing Cons: Greasy, patient's don't like them or comply

Question 60

Creams

Answer 60

Pros: Better patient compliance Cons: Less potent than ointments, and can sting on open skin

Question 61

Lotion or solutions

Answer 61

Pros: Better patient compliance Cons: They sting

Question 62

Foams

Answer 62

Pros: Good for scalp or hairy areas Cons: sting

Question 63

Gels

Answer 63

Pros: Good for intraoral use Cons: Drying and stinging

Question 64

Fingertip unit is

Answer 64

0.5 g of medication on the distal phalanx

Question 65

Psoriasis

Answer 65

Polygenic, autoimmune Flared by trauma, infection, medication ``` Plaque psoriasis (pink scales, symmetric and elbows and knees most common) Guttate psoriasis (numerous small lesions) Pustular psoriasis (erythema overlying pustules ``` Can have pinpoint pitting in the nail plate with yellow discoloration

Question 66

Psoriasis treatment

Answer 66

Corticosteroids, retinoids, coal tar derivatives Calcineurin derivatives Extensive or recalcitrant disease give phototherapy or systemic meds TNF-alpha inhibitors Do not give Oral corticosteroids since removal results in flare

Question 67

Atopic Dermatitis

Answer 67

Caused by profillagrin mutations (ichthyosis vulgaris patient predisposed, obviously) Secondary infection with staph aureus is common and can aggravate it (inflammation) Herpes simplex eczema can complicate it as well Acute edematous and erthematous papules and plaques that may ooze Chronic lesions will have lichenification Infantile is predominantly on the face, but spares the diaper area In childhood, the lesions are not as exudative, and flex points (antecubital and popliteral fossae) involved Adults AD has evidence of excoriation and rubbing Dry skin common (xerosis)

Question 68

Atopic dermatitis treatment

Answer 68

Emolliant application, corticosteroid topical treatments Antihistamines to relieve itch

Question 69

Seborrheic Dermatitis

Answer 69

Greasy, yellow scale on infant head (cradle cap) In kids it usually resolves with age. If it persists, may indicate patient has AD also. In adolescents and adults, in scalp/face in areas with significant sebum production Treat with emolliants, gentle skin care. Maybe use corticosteroids. Antifungals may help

Question 70

Lichen Planus

Answer 70

Autoimmune T cell mediated basal keratinocyte hypersensitivity Small, purple, polygonal, pruritic, planar papules and plaques Have Wickham's striae (lines) Wrists, forearms, shins. Also commonly hit buccal mucosa. Resolve on their own, but may need corticosteroids and antihistamines