Adnexal Structures and Associated Disorders Flashcards

1
Q

What are the 3 subunits of the hair shaft of the pilosebaceous unit?

A

infundibulum: (upper segment): refers to portion from the skin to the sebaceous gland

isthmus: (middlesegment) which extends from the point of insertion of the arrector pili muscle to the sebaceous gland

hair bulb: the hair shaft grows from this mitotically active undifferentiated cells of the matrix portion of the hair bulb

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2
Q

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

A

hair bulb

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3
Q

what are the 3 types of pilosebaceous units?

A
  1. Lanugo (fetal)
  2. Vellus (fine)
  3. Terminal (coarse)
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4
Q

What are two examples of abnormal hair type for age or location signifying an undlerlying cndition

A

Anorexia (Lanugo)

Hirsutism (Terminal)

*females with terminal hair in male patter distribution (beard) may indicate excess androgen/ polycystic ovarian syndrome (PCOS)

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5
Q

Sebaceous Glands

where

what

how

when

A

where? greatest density on face and scalp, but everywhere

what? Produce (oil) sebum.

*triglycerides, free ftty acids, squalene, wax and sterol esters, and free sterols

How? holocrine secretion

When? Active at birth, but decreases during infacny. Sebum production stimulated by androgen production (5-alpha-dihydrotestosterone) in uberty

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6
Q

What is the hair cycle?

A
  • Growth phase (anagen)
    • majority of hair on scalp, duration dictates hair length
  • Transition phase (catagen)
  • Resting phase (telogen)
    • hair shed during this phase
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7
Q

what is Telogen effluvium? what causes it?

A

Greater proportion of hair follicles (normally <15%) entering telogen phase (falling out)

**increase in hair shedding**

occurs approx 3 months after a stressful event, and slowly returns t normal. Could be pregnancy, broken bone, bad flu, psychosocial stress

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8
Q

What are club hairs?

A

instead of a typical hair bulb, you see a meek hair butt.

it is a hair follicle that is in telogen. It is a telogen bulb

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9
Q

What causes alopeci areata? What is it? How do we treat it?

A

autoimmune

smooth pathces of complete alopecia develop

nail pits (indentations in the nail plate) may be seen

topical corticosteroids are the mainstay of treatment

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10
Q

What is an eccrine gland and what innervates it? Where are they located?

A

sweaty gland

palms and soles

innervated by sympathetic fiber via Ach

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11
Q

What is an apocrine gland? Where are they located?

A

sweaty and smelly

axillae, anogenital, periumbilical, areolae, vermilion border of lips

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12
Q

What is hyperhidrosis?

A

overactive seat gland

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13
Q

what is anhidrosis/hypohidrosis?

A

occurs when sweat glands are absent/reduced

eg. ectodermal dysplasia

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14
Q

What are 3 disorders of the pilosebaceous unit?

A

acne vulgaris, acne rosacea, tinea veriscolor

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15
Q

How do sebaceous cells and follicular keratinocytes lead to the production of microcomedos?

A
  • Sebaceous cells
    • sebum
    • fatty acids
  • Follicular keratinocyte
    • hyperproliferation
    • keratohyaline granules increase
    • disturbed desquamation
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16
Q

Once a microcomedo is formed from the interaction of sebaceous cells and follicular keratinocytes what happens?

A

either closed comedo, open comedo or inflammatory lesions

17
Q

How do we form an open or closed comedo from a microcomedo?

A

sebum accumulates

follicle enlarges

keratinous material builds up

***closed=white, open=black. black is oxidized.

18
Q

How do inflammatory lesions form from a microcomedo?

A

P acnes (bacteria) and immune reactions

19
Q

How do androgens (testosterone and DHT) influence microcomedo production

A

they increase sebum production and hyperproliferation. therfore increasing microcomedo production

20
Q

Describe the pathogenesis of acne

A
  • Proprionibacterium acnes: releases enzymes that promote follicular rupture and stimulates the release of proinflammatory mediators leading to neutrophil recruitment and Th1 responses.
  • anaerobic gram positive rod
  • dependent on glycerol: hydrolysis of sebum triglycerides
  • produce:
    • porphyrins
    • proinflammatory mediators
    • lipases
21
Q

Hoe do retinoids treat acne?

A

they target the comedone which is the inciting lesion of acne.

they work via:

  • normalization of follicular keratinization, expulsion of existing kertinaceous follicular plugs, and prevention of the formation of new lesions
22
Q

How does Benzoyl peroxide treat acne?

A

It kills the bacteria P acnes that leads to inflammatory lesions

23
Q

How do antibiotics treat acne?

A

they kill P acnes!

24
Q

What 3 things are used for systemic treatment of acne?

A

antibiotics

oral contraceptives

isotretinoin

25
Q

What antibiotics are used for systemic acne treatment?

A
  • first line=tetracyclines
  • sometimes use: erythromycin, bactrim, penicillins
26
Q

How does the tetracycline family treat acne and what are the side effects?

A
  • tetracycline, doxycycline, minocyclin
  • mechanism: inhibition of P. acnes
  • antiinflammatory: decreases proinflammatory mediators
  • side effects:
    • doxycycline: pill esophagitis, photosensitivity
    • minocyclineL drug hypersensitivity syndorme, drug-induced lupus, hepatitis
27
Q

How are oral contraceptives used to treat acne?

A
  • Mechansim
    • block production of androgens: adrenal and ovarian
    • increase sex-hormone binding globulin=decreased free testosterone
  • type of acne:
    • inflammatory papules/pustules
    • peri-menstral flare
  • side effects: nausea, vomiting, abnormal menses, weight gain, breast tenderness, thrombophlebitis
28
Q

What are the indications for isotretinoin and what is the appropriate dose?

A
  • Indication:
    • severe nodulocystic acne
    • scarring
    • severe acne recalcitrant to systemic antibiotic therapy and topicals
  • dose
    • cumulative dose 120-150 mg/kg
  • systemic retinoid, decrease sebum, anti-inflammatory, increase shedding
29
Q

What is Tinea versicolor aka Pityriasis versicolor

A
  • Malassezia spp (globosa and furfur)
  • oval to round scaly patches with fine overlying scale
  • hyperpigmented (brown) or hypopigmented (lighter in color)
30
Q

WHat are primary lesions for acne vugaris called?

A

papules (including comedones), pustules, nodules, cysts

31
Q

What can primary lesions for tinea versicolor be? How about seconary?

A

primary: macules, patches
secondary: color (hypo/hyper), scale

32
Q

Summary of Telogen effluvium:

A
  • patients note increase in hair shedding
  • diffuse hair thinning results; often subjective
  • no discrete patches of alopecia
  • secondary changes: (erythmea, scale) not common
33
Q

summary of alopecia areata

A

patches of hair loss (this is different from telogen effluvium), varibale in size, tends to be focal

secondary changes not common

34
Q

What commonly occurs after acne?

A

scarring, most commonly after inflammatory lesions

post-inflammatory hyperpigmentation (persist for months and often confused for uncontrolled acne)

35
Q

What is acne rosacea?

A

multifactorial but associated with vascular hyperreactivity

history of easy blushing, and over time develop a reddened complexion