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Dermatology > Dermatology Intro 2 > Flashcards

Dermatology Intro 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the functions of the hair? ( 6 )

A
  • Protection against external factors
  • Sebum
  • Apocrine sweat
  • Thermoregulation
  • Social and sexual
    interaction
  • Epithelial and melanocyte stem cells
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2
Q

What are Terminal hairs?

A

Hair on the scalp, eyebrows and eyelashes

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3
Q

What are Vellus hairs?

A

Rest of the body ( except palms, soles, lips, external genitalia )

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4
Q

Describe the three phases of the hair cycle

A

(85%) Anagen : new hair forms and grows 2-6 years

(1%) Catagen: regressing phase, 3 weeks

(10-15%) Telogen: resting phase, 3 months

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5
Q

Describe the structure of hair in the skin?

A

Pockets of epithelium continuous with superficial epidermis

Human skin contains pilosebaceous follicles and sweat glands.

Envelop a small papilla of dermis at their base.

Arrector pili (smooth muscle) extends at angle between surface of dermis and point in follicle wall.

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6
Q

What is the Holocrine sebaceous gland?

A

( sebaceous gland is a type of holocrine gland because it release sebum which is dead reminent of the gland itself )

Open up into pilary canal which drains into axillae. releases sebum

  • follicles are associated with aporcine glands
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7
Q

What is the infundibulum?

A

Uppermost portion of the hair follicle extending from opening of sebaceous gland to surface of the skin

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8
Q

What is the Isthmus?

A

Lower portion of upper part of hair follicle between opening of sebaceous gland and insertion of arrector pili muscle

  • between the infundibulum and suprabulbar region

Epithelium keratinization begins with lack of granular layer named

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9
Q

What is the bulge?

A

Segment of the outer root sheath located at insertion of arrector pili muscle
Hair follicle stem cells reside here

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10
Q

Why may the bulge migrate down?

A

Downward → generate the new lower anagen hair follicle → enter hair bulb matrix, proliferate and undergo terminal differentiation to form hair shaft and inner root sheath.

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11
Q

Why may the bulge migrate up?

A

Upwards (distally) → form sebaceous glands and to proliferate in response to wounding

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12
Q

What is the bulb?

A

Lower most portion of the hair follicle, includes the follicular dermal papilla and the hair matrix

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13
Q

What is the outer root sheath

A

Extends along from the hair bulb to the infundibulum and epidermis serves as a reservoir of stem cells
Inner root sheath

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14
Q

What is the Inner root sheath

A

Guides / shapes hair

Encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fiber and capillary loop.

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15
Q

What are the functions of the nails? ( 5 )

A

Protection of underlying distal phalanx

Counterpressure effect to pulp important for walking and tactile sensation

Increase dexterity / manipulation of small objects

Enhance sensory discrimination

Facilitate scratching or grooming

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16
Q

What is the nail plate?

A

Final product of proliferation and differentiation of nail matrix
keratinocytes

Emerges from proximal nail fold

Grows at 1-3mm/month

Firmly attached to nail-bed

Detaches at hyponychium

Lined laterally by lateral nail folds

17
Q

What does the nail matrix do?

A

Produces nail plate

Nail matrix keratinocytes differentiate → lose their nuclei and are strictly adherent - cytoplasm completely filled by hard keratins

Also contains melanocytes

Lies under proximal nail fold, above bone of distal phalanx (to which it is connected by a tendon

Lunula only visible proportion

18
Q

What are the characteristics of Psorasis?

A

Chronic, immune mediated disorder

Have polygenic predisposition but environmental trigger needed.

Demarcated, scaly, erythematous plaques

Common sites are scalp, elbows and knees, nails, hands, feet and trunk (including intergluteal fold)

19
Q

Describe the pathophysiology of Psoriasis

A

Keratinocytes put under ‘stress’ and release DNA

Forms complex with antimicrobial peptides

Induce cytokines - TNF-alpha, IL-1, IFN-alpha to activate dermal dendritic cells

dDCs go to lymph nodes, cause Th1, Th17, Th22 cells to release chemokines.

Inflammatory cells move into dermis and release their own cytokines

Results in keratinocyte proliferation - plaque

20
Q

What cause cause keratinocyte ‘stress’?

A

Trauma, pathogens

21
Q

What systemic manifestations may occur due to psoriasis?

A

Psoriatic arthritis is most common systemic manifestation - linked to nail psoriasis

Liver inflammation

22
Q

What is Guttate Psoriasis?

A

Follows a streptococcal throat infection

teardrop shapes rash

23
Q

How to manage Psoriasis?

A

Secondary prevention - stop aggrevating factors:

Alcohol, Smoking

Co-morbidities risk should be managed

Psychologist

( anti TNF

24
Q

What medication can be given for Psoriasis? - 1st line

A

First line : topical treatments - steroids, VD analogue, retinoids, topical tacrolimus/pimecrolimus

Phototherapy:

  • Narrowband UVB
  • PUVA (Psoralen + UVA) ( increased risk of skin cancer )
25
Q

What 2nd Line treatments are available for Psoriasis?

A

Acitretin

  • Systemic immunosuppression
  • Methotrexate
  • Ciclosporin

Advanced therapies
-PDE4 inhibitors (Apremilast) inhibits TNF
-Biologics (anti-TNF-α, anti-IL-17, anti-IL23) monoclonal antibodies
0JAK inhibitors

26
Q

What are the characteristics of Atopic Eczema?

A
  • Intensely pruritic chronic inflammatory condition
  • Complex genetic disease with environmental
    influences
  • Infancy or early childhood
  • Often associated with other ‘atopic’ disorders e.g. asthma, rhinoconjunctivitis
  • Acute inflammation of cheeks, scalp and extensors in infants
  • Flexural inflammation and lichenification in children and adults
  • Daily emollients and anti-inflammatory therapy are cornerstone of management
27
Q

Eczema barrier defect pathophysiology?

A
  • Filaggrin not working: bind and aggregate keratin bundles and intermediate filaments forming cellular scaffold in corneocytes
  • Reduced extracellular lipids and impaired ceramide production
  • Increased transepidermal water loss
  • Lack of protection from microbes and allergens
28
Q

Eczema immune dysregulation pathophysiology?

A
  • Staphylococcal superantigens stimulate Th2 lymphocyte
    responses and subvert T‐reg
  • T-cell infiltrate - bias towards Th2 responses

Role of microbiome?

Eosinophils

29
Q

Clinical features of Eczema(s)?

A

Infantile phase : Erythematous, Odematous pupale, plaques on face and limbs

Childhood/ adult : Lichenification, crusting, excoriation and dyspigmentation

Fissuring

Allergic contact dermatitis

Impetignisation - gold crust staphylococcus aureus

venous stasis eczema

30
Q

What is a clinical feature of emergency Eczema

A

Eczema herpeticum

Monomorphic Errosions in epidermis

31
Q

How to manage Atopic Eczema?

A
  • Emollients
  • Omission of soap
  • Clinical Nurse Specialist involvement
  • technique
  • Day treatment
  • Habit reversal
  • Co-morbidities
  • Patch testing
  • Biopsy ( nipple eczema may be cancer)
32
Q

What Topical Medicines are there for Eczema?

A
  • Topical corticosteroids - correct potency for correct site
  • Topical tacrolimus / pimecrolimus

Phototherapy:

  • Narrowband UVB
  • PUVA (hand dermatitis)
33
Q

Which topical steroids are available for eczema?

A

Least potent:

Hydrocortisone
Clobetasone
etamethasone
Mometasone
Clobestaol

Most potent

34
Q

2nd line management for Eczema?

A

Retinoids (hand dermatitis)

Systemic immunosuppression
Methotrexate
Ciclosporin
Azathioprine
Mycophenolate mofetil

Advanced therapies
Biologics (anti-IL-4α, anti-IL13)
JAK inhibitors

Dermatology (3 decks)

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