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Musculoskeletal and Skin Pathology > Adnexal Structures and Associated Disorders > Flashcards

Adnexal Structures and Associated Disorders Flashcards

1
Q

Lanugo hair

A

Fetal hair follices

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2
Q

Vellus hair

A

Very fine hair

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3
Q

Terminal hair

A

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

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4
Q

Pilosebaceous unit

A

Consists of hair follicle and its associated sebaceous gland

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5
Q

Holocrine secretion

A

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

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6
Q

Areas with sebacious glands without accompanied hair

A

Nipples, eyelids, orogenital tract

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7
Q

Anagen phase

A

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

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8
Q

Catagen phase

A

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

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9
Q

Telogen phase

A

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

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10
Q

Growth phase variation?

A

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

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11
Q

Telogen effluvium

A

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.

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12
Q

Alopecia areata

A

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

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13
Q

Anagen effluvium

A

Chemo/drug induced hair loss.

2-3 weeks post-drug administration

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14
Q

Eccrine glands

A

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

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15
Q

Eccrine gland sweat product

A

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

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16
Q

Eccrine gland function

A

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.

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17
Q

Apocrine glands

A

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.

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18
Q

Acne Vulgaris

A

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

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19
Q

How does adrenarche contribute to acne?

A

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

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20
Q

Main things in non-inflammatory acne?

A

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

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21
Q

Main things in inflammatory acne?

A

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.

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22
Q

How do retinoids target comedones?

A

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

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

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23
Q

Antiinflammatories for acne?

A

Benzoyl peroxide, clindamycin and erythromycin

Also function as P. acnes antibiotics.

Orally active drugs include doxycycline and minocycline

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24
Q

Acne rosacea

A

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

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25
Q

Melanocytes

A
  1. Derived from neural crest
  2. Basal layer of epidermis.
  3. Release melanin
    Ratio of melanocytes to keratinocytes is 1:10
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26
Q

Vitiligo

A

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

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27
Q

Albinism

A

Defect in melanin production (cutaneous or oculocutaneous)

Decreased visual acuity and nystagmus common

High skin cancer risk

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28
Q

Piebaldism

A 
Autosomal dominant
White patches (poliosis), and skin
SEctions of skin or hair lacking melanocytes
Stable condition that does not progress.
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29
Q

Waardenburg Syndrome

A 
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)
30
Q

Melanocytic nevi

A

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

31
Q

Congenital melanocytic nevi

A

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

32
Q

Ephelides

A

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

33
Q

Cafe-au-lait spots.

A

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

34
Q

Solar lentigo

A

Dark brown or black macules due to UV light.

Later in life, larger (5-15 mm in size)

Chronic sun exposure.

35
Q

Dermal melanocytosis

A

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

36
Q

Acanthosis nigricans

A

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)

37
Q

Diabetic dermopathy

A

A marker for poor diabetes control. Brown, atrophic macules on the shins.

Trauma may set them off.

38
Q

Necrobiosis lipoidica diabeticorum

A

Shins of diabetic patients
Yellow orange atrophic patches
Expand into ulcerations

No association with diabetic control

39
Q

Diabetic Bullae

A

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

40
Q

Hyperthyroid derm effects

A

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

41
Q

Hypothyroidism derm effects

A

Dry, rough skin

Loss of lateral third of eyebrow hair

42
Q

Cushing’s derm effect

A

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

43
Q

Addison’s disease derm effects

A

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

44
Q

Prophyria cutanea tarda

A

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

45
Q

Lupus flares

A

Usually photosensitive. Lupus in general more common in females

46
Q

Systemic Lupus erthematosus

A

Multisystem form. Malar/butterfly rash

Accompanied by alopecia, oral ulcers, raynaud phenomenon

47
Q

Discoid lupus erythematosus

A

Minority of SLE patients. Skin limited (not multiorgan)

Hyperkeratotic, violaceous plaques

Head and neck, scalp and ears

Atrophic scarring

48
Q

Subacute cutaneous lupus erythematous

A

Skin-limited, associated with internal disease sometimes

Pink scales on sun-exposed skin

49
Q

How to treat lupus?

A

Corticosteroids

50
Q

Dermatomyositis

A

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)

51
Q

Sarcoidosis

A

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

52
Q

Dermatitis Herpetiformis

A

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

53
Q

Neurofibromatosis Type I

A

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)

54
Q

Tuberous Sclerosis

A

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)

55
Q

Sturge-Weber Syndrome

A

Port wine stain (capillary malformation) present at birth on opthalmic trigeminal distribution

Cerebral calcifcation and seizure

Glaucoma ipsilaterally

56
Q

PHACE syndrome

A 
Posterior fossa brain malformation
Hemangiomas on face
Arterial cerebrovascular anomalies
Cardiovascular anomalies
Eye anomalies
57
Q

Topical corticosteroids

A

All from glucorticoid family. Anti-inflammatory

58
Q

Steroid side effects

A

Reversible: hypopigmentation, hypertrichosis, skin atrophy, telangiectasia

Irreversible: Striae

Allergies also possible

59
Q

Ointments

A

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

60
Q

Creams

A

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

61
Q

Lotion or solutions

A

Pros: Better patient compliance
Cons: They sting

62
Q

Foams

A

Pros: Good for scalp or hairy areas
Cons: sting

63
Q

Gels

A

Pros: Good for intraoral use
Cons: Drying and stinging

64
Q

Fingertip unit is

A

0.5 g of medication on the distal phalanx

65
Q

Psoriasis

A

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

66
Q

Psoriasis treatment

A

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

67
Q

Atopic Dermatitis

A

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)

68
Q

Atopic dermatitis treatment

A

Emolliant application, corticosteroid topical treatments

Antihistamines to relieve itch

69
Q

Seborrheic Dermatitis

A

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

70
Q

Lichen Planus

A

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

Musculoskeletal and Skin Pathology (10 decks)

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