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BRS Dermatology > Dermatology Pt 2 > Flashcards

Dermatology Pt 2 Flashcards

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Dermatology Board Prep flashcards
1
Q

Give 6 of the functions of the hair

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

What are the two types of hair?

A

Vellus and terminal

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3
Q

Where is vellus hair found?

A

Rest of body except for: palms, soles, mucosal regions of lips and external genitalia

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4
Q

Where is terminal hair found?

A

Scalp, eyebrows and eyelashes

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5
Q

What are the 3 steps of the hair cycle and what happens in each of them?

A

Anagen - where new hair forms and grows
85% of hair; lasts 2-6 years

Catagen - regressing phase
1% of hair; lasts 3 weeks

Telogen - resting phase
10-15% of hair; lasts 3 months

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6
Q

What is the pilosebaceous unit also known as?

A

Hair follicle

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7
Q

What is the function of the Arrector Pili?

A

Contracts to make the hair erect on the skin to generate heat

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8
Q

Outline the structure of hair.

A

Human skin contains pilosebaceous follicles and sweat glands.

Hair follicles

Pockets of epithelium continuous with superficial epidermis.

Envelop a small papilla of dermis at their base.

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9
Q

Where do the holocrine sebaceous glands open up into?

A

The pilary canal → in axillae

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10
Q

Where are apocrine glands found?

A

In the skin are in the armpits, the groin, and the area around the nipples of the breast

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11
Q

What is the uppermost portion of the hair follicle called?

A

Infundibulum - extends from opening of sebaceous gland to surface of the skin

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12
Q

What is the lower portion of the hair follicle called and what happens here?

A

Isthmus - Between opening of sebaceous gland and insertion of arrector pili muscle.

Epithelium keratinisation begins with lack of a granular layer - Trichilemmal keratinisation

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13
Q

What is meant by keratinaztion?

A

The cytoplasmic events that take place in keratinocytes that move through the different layers of the epidermis to finally differentiate to corneocytes.

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14
Q

What is found in the Bulge of the hair?

A

Hair follicle stem cells

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15
Q

Where and in what manner do these hair stem cells migrate?

A

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

Upwards (distally) - form sebaceous glands and to proliferate in response to wounds

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16
Q

What is the hair bulge?

A

Segment of outer root sheath located at insertion of the APM.

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17
Q

What is the hair bulb?

A

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

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18
Q

Where is the outer root sheet (ORS)?

A

Extends from the hair bulb to the infundibulum and epidermis.
Serves as a reservoir for stem cells.

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19
Q

What is the purpose of the IRS?

A

Guides/shapes hair

Encloses follicular dermal papilla, mucopolysaccharide-rich stroma, nerve fibre and capillary loop > Structural support

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20
Q

Give 5 of the functions of the nails

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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21
Q

Where does the nail plate emerge from?

A

Proximal nail fold

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22
Q

How fast does a nail grow?

A

1-3mm/month

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23
Q

Where does the nail plate detach?

A

Hyponychium

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24
Q

What is the nail plate lined laterally by?

A

Lateral nail folds

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25
Q

What produces the nail plate?

A

Nail matrix

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26
Q

Where is the nail matrix found?

A

Under proximal nail fold, above bone of distal phalanx

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27
Q

What is the only visible portion of the nail matrix called?

A

Lunula

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28
Q

What occurs in the nail matrix?

A

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

Also contains melanocytes

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29
Q

Is polygenic predisposition enough to contract Psoriasis?

A

No, environmental triggers are also needed (e.g. trauma, infections or medications

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30
Q

What is the most common form of Psoriasis characterised by?

A

Sharply demarcated, scaly, erythematous plaques

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31
Q

What are the common sites of involvement with Psoriasis?

A

Scalp, elbows and knees, followed by nails, hands, feet and trunk

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32
Q

What is the most common systemic manifestation of Psoriasis?

A

Psoriatic arthritis

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33
Q

Explain the pathophysiology of Psoriasis

A

Stressed keratinocytes release DNA/RNA which form complex with antimicrobial peptides (endogenous antibiotic - Psoriasin) Cathelicidins and defensins.

Induces release of cytokines - TNF-alpha, IL-1 and IFN-alpha

This activates dermal dendritic cells (dDCs)

dDcs migrate to the lymph nodes and promote Th1, Th17, Th22 cells

These release chemokines which cause the migration of inflammatory cells into the dermis

These inflammatory cells cause release of cytokines which lead to keratinocyte proliferation

This leads to a psoriatic plaque

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34
Q

Why do scales form on the skin during Psoriasis?

A

Keratin differentiation process occurs so quickly due to increased keratin proliferation that they do not differentiate correctly.

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35
Q

Why do you not see these same scales in Flexural Psoriasis?

A

The friction rubs it away as these tend to be in areas where the genitalia are.

36
Q

Name some of the features seen in Nail Psoriasis?

A

Subungal hyperkeratosis - scaling of the nail coming from the nail matrix

Onycholysis - nail lifts of nail bed

Pitting - Keratinocytes forming the nail plate are inflamed and not sticking to the other keratinocytes effectively

37
Q

When can the term ‘erythroderma’ be used to describe someone’s condition?

A

When 90% or more of their skin is inflammed

38
Q

What type of infection does Guttate Psoriasis typically follow?

A

Streptococcal throat infection

39
Q

What type of psoriasis manifests as read tear drops on body?

A

Guttate psoriasis

40
Q

What is meant by secondary prevention of a condition?

A

Minimisation or avoidance of the aggravating factors

41
Q

Give examples of some of these aggravating factors that might aggravate Psoriasis

A

Smoking and Alcohol consumption

42
Q

What co-morbidities might Psoriasis increase your risk of contracting?

A

Psoriatic Arthritis

Coronary Artery disease

Inflammatory Bone disease

43
Q

Give an example of a type of treatment that is used to treat both inflammatory bowel disease and psoriasis?

A

Anti-TNF biologic treatments

44
Q

What are some of the 1st line treatments considered when treating Psoriasis?

A

Topical gels, creams, ointments and foams or phototherapy

45
Q

What are some of the topical therapies that are used to treat psoriasis?

A

Vitamin D analgoues - calcipotriol

Topical coritcosteroids

Retinioids - Vitamin A analogues

Topical tacrolimus - T-cell inhibitors

46
Q

What does phototherapy do?

A

Induces T-Cell apoptosis

47
Q

Why might phototherapy be considered over topical therapies?

A

Cream cannot be constantly applied all over the body and so when the psoriasis covers more than 20% of the body’s surface area, phototherapy is used.

48
Q

Why would you be less likely to use PUVA over UVB?

A

UVB does not cause an increased risk of skin cancer, whereas PUVA does

49
Q

What are the 2 photo therapies used for psoriasis management?

A

Narrowband - UVB

PUVA (psoralen and UVA)

50
Q

What is Acitretin and why would it be used as a treatment for Psoriasis?

A

Oral retinoid - Vitamin A analogue

Retinoids help bring order to the differentiation of the keratinocytes from deep to superficial.
Therefore it restores order of keratinisation.

51
Q

Give 2 examples of immunosuppressive drugs used for psoriasis management and briefly explain what do they do?

A

Methotrexate - Anti-inflammatory effect

Ciclosporin - Inhibits T-cells

52
Q

What does Apremilast do?

A

It is a Phosphodiesterase (PDE4) inhibitor and this allows reduction in the amount of TNF.

53
Q

What are biologics when referring to the advanced treatments of Psoriasis?

A

Injected mABs against TNF-alpha, IL-17 and IL-23

54
Q

What are some of the other atopic disorders associated with atopic eczema?

A

Rhinoconjunctivitis which is Hay Fever

Asthma

55
Q

What is atopic eczema?

A

Intensely prurititc (itchy) chronic inflammatory condition
Complex genetic disease with environmental influences.
Typically begins during infancy or early childhood.

56
Q

Does flexural inflammation and lichenification occur in children or adults?

A

Both

57
Q

Where does acute inflammation occur in children with atopic eczema?

A

Acute inflammation of cheeks, scalp and extensors

58
Q

What cornerstones of atopic eczema management?

A

Daily emollients and anti-inflammatory therapy

59
Q

What does filaggrin do?

A

Binds and aggregatees keratin bundles and inetermediate filaments to form cellular scaffold in corneocytes.

60
Q

What conditions is eczema/dermatitis an umbrella term for?

A

Atopic eczema, seborrhoiec dermatitis, venous stasis eczema, allergic contact dermatitis, irritant contact dermatitis

61
Q

What role does Filaggrin play in the pathophysiology of eczema?

A

A defect in the genes coding for the protein means that it cannot function correctly
which means that the stratum corneum cannot function correctly, predisposing to eczema.
This means that the extracellular lipids and ceramide production at the stratum corneum are reduced.
Ceramide locks moisture into your skin and without this, there is a net effect of Transepidermal Water Loss (TEWL).
This leads to impaired protection against microbes and environmental allergens.

62
Q

How can immune dysregulation lead to eczema?

A

Staphylococcal superantigens stimulate Th2 lymphocyte responses and subvert T-reg

Cytokine release leads to epidermal lichenification, spongiosis, decreased filaggrin.

63
Q

What symptoms result from atopic eczema in children?

A

Erythematous, oedematous papule and plaques with/without vesiculation

64
Q

Into adulthood, what symptoms are found due to atopic eczema?

A

Lichenification due to chronic scratching, exaggeration of the normal skin markings and disordered pigmentation

65
Q

What is fissuring?

A

Loss of hydration of the epidermis and so it becomes less flexible and cracks

66
Q

What 3 things can be seen in people with allergic contact dermatitis/eczema?

A

Poison Ivy

Nickel - Ear piercing

Cobalt - Inner shoe lining

67
Q

What is impetiginisation?

A

Gold crust due to S.aureus infection.

68
Q

What is seen in venous stasis eczema?

A

Swollen legs

Keratinocytes no longer functional > Barrier lost

69
Q

How would you describe an ‘erosion’?

A

Breaches in the epidermis that don’t go all the way through (if they did, that would be an ulcer)

70
Q

What happens if Eczema Herpeticum is left untreated?

A

It can be complicated by encephilitis, blindness and can be fatal

71
Q

What lifestyle modifications could be applied to manage atopic eczema?

A

Moisturise at least 3 times a day

Omission of soap

Habit reversal of scratching

Clinical nurse specialist involvement for topical application technique, day treatment, habit reversal.

Co-morbidities: Patch testing + Biopsy

72
Q

Why might patch testing be used to manage atopic eczema?

A

Patch testing is used to detect allergies

These allergies could be what is aggrevating the eczema if treatment is not working on the eczema

73
Q

If someone who has nipple eczema is not responding to treatment, why would you take a biopsy?

A

Paget’s disease of the nipple is associated with underlying breast cancer which looks exactly the same as nipple eczema

Could also be a skin lymphoma

74
Q

What topical therapies can be given to manage eczema?

A

These are 1st line treatments:
Topical corticosteroids - correct potency for correct site
Topical tacrolimus / pimercrolimus - T-cell inhibitor

75
Q

What case would PUVA be used in eczema management?

A

Hand dermatitis

76
Q

What is meant by a fingertip unit?

A

The amount of topical steroid that is squeezed out from a standard tube along an adults fingertip

77
Q

Are perioral dermatitis and rebound syndrome (tachyphylaxis), rare, very rare or extremely rare adverse effects of topical corticosteroids?

A

Very rare

78
Q

Are skin atrophy, exacerbation of acne and rosacea, and infection, rare very rare or extremely rare adverse effects of topical corticosteroids?

A

Rare

79
Q

What are the extremely rare adverse effects of the topical corticosteroids?

A

Hormonal imbalance (Suppression of hypothalamic-pituitary-adrenal axis) and hirsuitism

80
Q

In what region of the body do retinoids work well against eczema in than others?

A

Hands

81
Q

Methotrexate, Ciclosporin, Azathioprine and Mycophenolate mofetil are examples of waht kind of drug that is used against eczema?

A

Systemic immunosuppression

82
Q

What are the biologics that are used in eczema management target?

A

IL-4 alpha

IL-13

83
Q

Give an example of one of these drugs.

A

Dupilimab

84
Q

What other condition is dupilimab used for?

A

Asthma

85
Q

Outline the topical steroid ladder (list of drugs from least to most potent)

A 
Hydrocortisone 
Clobetasone (eumovate)
Betamethasone (betnovate)
Mometasone (elocon) 
Clobetasol (dermovate)

BRS Dermatology (2 decks)

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