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SMP - APP Part 2 > Lectures 13 & 14 - Dermatology Pathophysiology I & II > Flashcards

Lectures 13 & 14 - Dermatology Pathophysiology I & II Flashcards

1
Q

4 functions of skin?

A
  1. Protection
  2. Body temperature regulation
  3. Sensation
  4. Others: vitamin D metabolism, some waste elimination through sweat
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2
Q

3 protections the skin provides? Describe each.

A
  1. Chemical: secretes antimicrobial chemicals in sweat, UV protection (via melanin secretion)
  2. Physical: waterproof barrier
  3. Biological: immune protecting cells in skin respond to invasion, normal flora
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3
Q

How does skin regulate body temperature?

A
  • Sweating when hot

- Blood vessels direct blood away from skin when cold

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4
Q

What sensations does the skin feel?

A
  1. Various nervous receptors in the dermis sense pressure, pain, temperature
  2. Hair movement sensed by hair follicle receptors
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5
Q

Describe the microanatomy of skin.

A
  1. Epidermis: keratinized stratified squamous epithelium to protect from abrasion and waterproof
  2. Dermis: connective tissue
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6
Q

Describe the basale layer of the epidermis.

A

Single, most deep layer of the epidermis, that contains melanocytes and is mitotic

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7
Q

Does the epidermis of the skin have a blood supply?

A

NOPE - nutrients via diffusion

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8
Q

What is the hypodermis?

A

Subcutaneous tissue with fat

Not part of skin

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9
Q

Is skin the only epithelium to be keratizined?

A

YUP

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10
Q

What does “keratinized” means?

A

With an outer later of keratin and other proteins and dead cells called the corneum

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11
Q

How many epidermal layers?

A

4-5 (5 for thick skin on palms and soles)

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12
Q

Layers of epidermis? List from deep to superficial.

A
  1. Stratum basale
  2. Stratum spinosum
  3. Stratum granulosum
  4. Stratum lucidum (only present in thick skin)
  5. Stratum corneum
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13
Q

Does the epidermis receive sensory innervation?

A

NOPE

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14
Q

How to skin cells desquamate?

A

As cells move away from the dermis, they receive less and less nutrients via diffusion and begin to die off

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15
Q

What is found in the dermis? 4

A
  1. Sweat glands
  2. Hair follicles
  3. Blood vessels
  4. Touch receptors
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16
Q

2 types of layers of the dermis? List from deep to superficial and describe them.

A
  1. Reticular layers: dense and irregular connective tissue (fibers angled in different directions), allowing for skin to be pulled in multiple directions
  2. Papillary layers: forming dermal papillae ridges and containing areolar connective tissue (fluffy cushion)
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17
Q

What are the dermal papillae important for?

A

They form finger prints and help with grip

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18
Q

Which is packed more tightly: dermis or epidermis?

A

Epidermis

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19
Q

3 ways to examine skin lesions?

A
  1. History:
    - Exposure and medication use
    - Onset, duration, and progression of lesions
    - Lesion characteristics: painful, itchy etc.
  2. Inspection:
    - Description of lesion type, shape, color etc.
    - Distribution
    - Progression
  3. Palpation:
    - Lesion raised, flat, etc.
    - Subcutaneous lesions
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20
Q

What is a macule?

A

Flat discolored lesion, < 1 cm in diameter

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21
Q

What is a patch?

A

Flat discolored lesion, >1cm in diameter

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22
Q

What is a papule?

A

Elevated (palpable) lesion, < 1cm in diameter

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23
Q

What is a plaque?

A

Elevated (palpable) lesion(s), > 1cm in diameter

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24
Q

What is a nodule?

A

Elevated, deep lesion with spherical edge, > 1cm in diameter

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25
Q

What is a vesicle?

A

Fluid-filled lesion, elevated, < 1 cm in diameter

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26
Q

What is a bulla?

A

Fluid-filled lesion, elevated, > 1 cm in diameter

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27
Q

What is a pustule?

A

Puss-filled lesion, variable size

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28
Q

What is a wheal? Other name?

A

Transient (<24 hours and shape changes), pruritic, elevated lesion with varying erythema (does not break the surface of the skin)

= hive

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29
Q

What is an excoriation?

A

Lesion after repeated scratching

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30
Q

What is a lichenification?

A

Thickening and roughing of skin after repeated rubbing/irritation

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31
Q

What is an erosion/ulceration?

A

Loss of epidermal/dermal components

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32
Q

What is a scale?

A

Dry flakes of keratin

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33
Q

Classic pustule?

A

Pimple

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34
Q

Name of tick bite lesion?

A

Bullseye lesion with central and outside erythemas

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35
Q

Skin lesions in shingles? What causes this?

A

Dermatomal linear distribution of papulovesicular lesions with erythematous base

Reactivation of herpes varicella zoster virus

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36
Q

Skin lesion in lupus?

A

Malar or butterfly rash

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37
Q

What is characteristic of secondary bacterial infections of skin lesions?

A

Golden crust

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38
Q

Skin lesion in superficial fungal infection? What is this called?

A

Flat hypopigmented lesion = tenia versicolor

= dermatophyte

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39
Q

Skin lesion in idiopathic thrombocytopenic purpura (ITP)?

A

Small bruise-like spots = petechiae all throughout the body

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40
Q

Skin lesions due to increased thoracic pressure?

A

Petechiae around eyes

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41
Q

2 types of dermatopathologies?

A
  1. Inflammatory dermatoses

2. Blistering diseases

42
Q

2 types of inflammatory dermatoses?

A
  1. Acute (days-weeks)

2. Chronic (months-years)

43
Q

Example of acute inflammatory dermatosis?

44
Q

3 examples of chronic inflammatory dermatoses?

A
  1. Psoriasis
  2. Seborrheic dermatitis
  3. Atopic dermatitis
45
Q

Other name for hives?

46
Q

Skin lesion in impetigo?

A

Eczematous rash, suprainfection

47
Q

Pathogenesis of hives? What to note?

A

Mast cell degranulation (histamine) and microvascular permeability and is either direct or IgE-mediated (attached to mast cells) (allergies) => reaction in superficial dermis

NOTE: mast cells not implicated in some causes: sunlight, cold, NSAIDs, hormones, infections

48
Q

Clinical manifestation of hives?

A

Episodes of pruritic wheals that fade within 24 hours with lesions that may coalesce into larger plaques

49
Q

Is the cause of hives known in most cases?

50
Q

8 possible causes of hives?

A
  1. Drugs (NSAIDs, opioids, muscle relaxants)
  2. Allergens (including foods)
  3. Infections (parasitic)
  4. Transfusion
  5. Insect bites
  6. Hormones
  7. Sunlight
  8. Cold
51
Q

Can hives be chronic?

52
Q

What are hives related to?

A

Related to angioedema: edema of the deeper dermis and subcutaneous tissue (most severely in the airways)

53
Q

Effects of histamine?

A
  1. Vasodilation

2. Itching

54
Q

Histological characteristic of hives?

A
  1. Superficial dermal edema (widening of spaces that separate the collagen bundles)
  2. Dilated lymphatic and blood-filled vascular spaces
55
Q

Treatment for hives?

A

Antihistamines

56
Q

Word origin of eczema?

A

To boil over

57
Q

What is eczematous dermatitis? What to note?

A

Broad class of skin conditions with oozing (wet) papulovesicular lesions, scaling (hyperkeratosis), and epidermal hyperplasia (acanthosis)

NOTE: can become superinfected

58
Q

2 subtypes of eczematous dermatitis?

A
  1. Contact dermatitis

2. Atopic dermatitis

59
Q

What is atopic dermatitis more commonly known as

60
Q

2 types of contact dermatitis? Describe each. Which is more common? Why?

A
  1. Allergen induced: immune mediated (cells on skin surface), delayed type hypersensitivity (sensitization and challenge) with plants (poison ivy), nickel, perfumes, latex etc.
  2. ***Irritant induced: direct damage to skin by irritant, non-immune mediated with workplace chemical exposure (acids, bleach, cement etc), diaper rash, prolonged water exposure, etc. (more common because all individuals will have a reaction)
61
Q

Cause of contact dermatitis?

A

Topically applied antigens

62
Q

Cause of atopic dermatitis?

A

Unknown; may be heritable (more common when there is a family history of eczema, hay fever, or asthma)

63
Q

Histology of ALL eczematous dermatitis types?

A

Spongiotic dermatitis = epidermis filled with fluid

64
Q

Clinical features of contact dermatitis?

A

Marked itching, burning, or both

65
Q

Clinical features of atopic dermatitis?

A

Erythematous plaques in flexural areas

66
Q

What is atopic dermatitis?

A

Chronic dermatosis

67
Q

What is the atopic triad?

A
  1. Asthma
  2. Allergic rhinitis
  3. Eczema
68
Q

Pathophysiology of atopic eczema?

A
  1. Immune system involvement: spongiosis = epidermis collects fluid in interstitial space => keratinocytes moved apart => weeping lesions and vesicles + simultaneous or subsequent scaling
  2. Dysfunctional epidermal permeability barrier: decreased ability to maintain hydration (due to a number of proteins implicated)
69
Q

When do atopic eczema flares tend to happen? Why?

A

Winter because skin is dryer

70
Q

When does atopic eczema usually start? What to note?

A

Early childhood (before age 5)

NOTE: usually appears on the face and usually improves with age

71
Q

Characteristic lesions of atopic eczema?

A
  1. Itchy
  2. On flexure surfaces
  3. Dry skin
72
Q

How to treat atopic eczema? What to note?

A
  1. Avoid epidermal disruption: avoid skin drying agents (e.g. low humidity, excess washing) and maintain hydration with thick creams with low water content
  2. Active lesions treated with topical steroids and anti-histamines for itching

NOTE: steroids can thin skin out and make it more dry

73
Q

What is psoriasis?

A

Chronic inflammatory dermatitis that can present alone or be associated with other joint or muscle diseases and have nail involvement

74
Q

What is most common type of psoriasis? Describe it. How many patients have this type?

A

Plaque psoriasis: pink plaques with erythematous base covered in thick silver scale (hyperkeratosis), most commonly on knees, elbows, scalp, lower back with multiple bleeding points when scale is removed (Auspitz sign)

> 80-90% of patients have this variant

75
Q

Pathogenesis of psoriasis?

A
  1. Immune mediated reaction with genetic association:
    - T cells and dendritic cells (immune cells in skin)
    - Immune mediated growth of keratinocytes in epidermis
    - Neutrophil microabscesses in superficial epidermal layers
  2. Hyperproliferation of epidermal cells => increased mitosis, even above basale layer => increased cell turnover and epidermal thickening
  3. Thinning of cellular epidermal layers near dermal papillae and dilation of blood vessels => papillae closer to skin surface => Auspitz sign
76
Q

Clinical presentation of psoriasis?

A

Presentation usually in early adulthood with characteristic lesions and may remit

77
Q

Treatment for psoriasis?

A
  1. Topical corticosteroids and lotions

2. Systemic immune targeting therapy for severe disease

78
Q

What can worsen psoriasis?

A

Some drugs can worsen disease or cause psoriasis-like reaction

79
Q

What are psoriasis associated conditions?

A
  1. Metabolic syndrome
  2. MI
  3. IBD
  4. Arthritis
80
Q

Does psoriasis affect mortality?

A

Usually not

81
Q

What does the severity of psoriasis depend on?

A

Coverage of the skin:

  1. Mild: < 3% of body
  2. Moderate: 3-10% of body
  3. Severe: > 10% of body
82
Q

What is seborrheic dermatitis? What to note?

A

Chronic dermatitis associated with skin high in sebaceous glands, which produce oil and are associated with hair follicle => maculopapular rash on greasy base with scaling and crusting on chest, armpits, forehead, scalp (dandruff, cradle cap in infants), nasolabial folds, genitals

NOTE: not a disease of sebaceous glands

83
Q

What % of population is affected by seborrheic dermatitis?

84
Q

Other name for seborrheic dermatitis?

85
Q

Is dandruff considered seborrheic dermatitis?

86
Q

2 histological features of seborrheic dermatitis?

A
  1. Scale with mild epidermal inflammation

2. Increased features around hair follicles

87
Q

Cause of seborrhea?

A

Unknown, but maybe increased sebum production, or lipophilic yeast colonization (Malassezia furfur)

88
Q

Treatment for seborrhea?

A
  1. Dandruff shampoo: anti-proliferative, anti-fungal

2. Topical corticosteroids if shampoo does not work

89
Q

What are blistering diseases?

A

Diseases in which blisters are the primary and distinctive feature:

  1. Pemphigus vulgaris
  2. Bullous pemphigoid
90
Q

In what conditions can blisters be seen? What to note?

A
  1. Burns
  2. Infections
  3. Eczema
  4. Trauma
  5. Blistering diseases

NOTE: blisters can form at many levels of skin and hence have different clinical features

91
Q

Are blistering diseases common?

92
Q

Difference between desmosomes and hemidesmosomes?

A

Desmosomes connect cells to each other

Hemidesmosomes are located at the basal surface and connect cells to the ECM

93
Q

What is pemphigus?

A

Rare autoimmune blistering disorder with loss of desmosomes => vesicles and bullae that rupture easily upon touching (Nikolsky sign) => leave erosions in skin

94
Q

Most common type of pemphigus?

A

Pemphigus vulgaris

95
Q

Can pemphigus be life-threatening?

96
Q

Treatment for pemphigus and bullous pemphigoid?

A

Systemic steroids or other immunosuppressives

97
Q

Pathogenesis of pemphigus? What to note?

A
  1. IgG antibody attack on desmoglein 3, which is a component in desmosomes at deeper layers of epidermis
  2. Acantholysis = lysis of intercellular adhesion
  3. Formation of suprabasal blisters above basale layer of epidermis

NOTE: basement membrane and dermal-epidermal junction intact => tomb-stone sign in histology because basal layer cells remain attached to the dermis

98
Q

What is bullous pemphigoid?

A

Autoimmune bullous disorder forming tense blisters (2-8 cm) that do not rupture and can heal without scarring

99
Q

Pathogenesis of bullous pemphigoid? What to note?

A
  1. Antibody attack on hemidesmosomes (bullous pemphigoid antigens 1 and 2) at dermal-epidermal junction (basement membrane-basale cell layer)
  2. Subepidermal blisters have tough epidermal covering
100
Q

Immunofluorescence pattern of Pemphigus?

A

Fishnet/mesh

101
Q

Immunofluorescence pattern of bullous pemphigoid?

A

Linear along the dermal-epidermal junction

SMP - APP Part 2 (7 decks)

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