Lectures 13 & 14 - Dermatology Pathophysiology I & II Flashcards

(101 cards)

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
What is a vesicle?
Fluid-filled lesion, elevated, < 1 cm in diameter
26
What is a bulla?
Fluid-filled lesion, elevated, > 1 cm in diameter
27
What is a pustule?
Puss-filled lesion, variable size
28
What is a wheal? Other name?
Transient (<24 hours and shape changes), pruritic, elevated lesion with varying erythema (does not break the surface of the skin) = hive
29
What is an excoriation?
Lesion after repeated scratching
30
What is a lichenification?
Thickening and roughing of skin after repeated rubbing/irritation
31
What is an erosion/ulceration?
Loss of epidermal/dermal components
32
What is a scale?
Dry flakes of keratin
33
Classic pustule?
Pimple
34
Name of tick bite lesion?
Bullseye lesion with central and outside erythemas
35
Skin lesions in shingles? What causes this?
Dermatomal linear distribution of papulovesicular lesions with erythematous base Reactivation of herpes varicella zoster virus
36
Skin lesion in lupus?
Malar or butterfly rash
37
What is characteristic of secondary bacterial infections of skin lesions?
Golden crust
38
Skin lesion in superficial fungal infection? What is this called?
Flat hypopigmented lesion = tenia versicolor = dermatophyte
39
Skin lesion in idiopathic thrombocytopenic purpura (ITP)?
Small bruise-like spots = petechiae all throughout the body
40
Skin lesions due to increased thoracic pressure?
Petechiae around eyes
41
2 types of dermatopathologies?
1. Inflammatory dermatoses | 2. Blistering diseases
42
2 types of inflammatory dermatoses?
1. Acute (days-weeks) | 2. Chronic (months-years)
43
Example of acute inflammatory dermatosis?
Hives
44
3 examples of chronic inflammatory dermatoses?
1. Psoriasis 2. Seborrheic dermatitis 3. Atopic dermatitis
45
Other name for hives?
Urticaria
46
Skin lesion in impetigo?
Eczematous rash, suprainfection
47
Pathogenesis of hives? What to note?
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
Clinical manifestation of hives?
Episodes of pruritic wheals that fade within 24 hours with lesions that may coalesce into larger plaques
49
Is the cause of hives known in most cases?
NOPE
50
8 possible causes of hives?
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
Can hives be chronic?
YUP
52
What are hives related to?
Related to angioedema: edema of the deeper dermis and subcutaneous tissue (most severely in the airways)
53
Effects of histamine?
1. Vasodilation | 2. Itching
54
Histological characteristic of hives?
1. Superficial dermal edema (widening of spaces that separate the collagen bundles) 2. Dilated lymphatic and blood-filled vascular spaces
55
Treatment for hives?
Antihistamines
56
Word origin of eczema?
To boil over
57
What is eczematous dermatitis? What to note?
Broad class of skin conditions with oozing (wet) papulovesicular lesions, scaling (hyperkeratosis), and epidermal hyperplasia (acanthosis) NOTE: can become superinfected
58
2 subtypes of eczematous dermatitis?
1. Contact dermatitis | 2. Atopic dermatitis
59
What is atopic dermatitis more commonly known as
Eczema
60
2 types of contact dermatitis? Describe each. Which is more common? Why?
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
Cause of contact dermatitis?
Topically applied antigens
62
Cause of atopic dermatitis?
Unknown; may be heritable (more common when there is a family history of eczema, hay fever, or asthma)
63
Histology of ALL eczematous dermatitis types?
Spongiotic dermatitis = epidermis filled with fluid
64
Clinical features of contact dermatitis?
Marked itching, burning, or both
65
Clinical features of atopic dermatitis?
Erythematous plaques in flexural areas
66
What is atopic dermatitis?
Chronic dermatosis
67
What is the atopic triad?
1. Asthma 2. Allergic rhinitis 3. Eczema
68
Pathophysiology of atopic eczema?
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
When do atopic eczema flares tend to happen? Why?
Winter because skin is dryer
70
When does atopic eczema usually start? What to note?
Early childhood (before age 5) NOTE: usually appears on the face and usually improves with age
71
Characteristic lesions of atopic eczema?
1. Itchy 2. On flexure surfaces 3. Dry skin
72
How to treat atopic eczema? What to note?
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
What is psoriasis?
Chronic inflammatory dermatitis that can present alone or be associated with other joint or muscle diseases and have nail involvement
74
What is most common type of psoriasis? Describe it. How many patients have this type?
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
Pathogenesis of psoriasis?
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
Clinical presentation of psoriasis?
Presentation usually in early adulthood with characteristic lesions and may remit
77
Treatment for psoriasis?
1. Topical corticosteroids and lotions | 2. Systemic immune targeting therapy for severe disease
78
What can worsen psoriasis?
Some drugs can worsen disease or cause psoriasis-like reaction
79
What are psoriasis associated conditions?
1. Metabolic syndrome 2. MI 3. IBD 4. Arthritis
80
Does psoriasis affect mortality?
Usually not
81
What does the severity of psoriasis depend on?
Coverage of the skin: 1. Mild: < 3% of body 2. Moderate: 3-10% of body 3. Severe: > 10% of body
82
What is seborrheic dermatitis? What to note?
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
What % of population is affected by seborrheic dermatitis?
1-3%
84
Other name for seborrheic dermatitis?
Seborrhea
85
Is dandruff considered seborrheic dermatitis?
YUP
86
2 histological features of seborrheic dermatitis?
1. Scale with mild epidermal inflammation | 2. Increased features around hair follicles
87
Cause of seborrhea?
Unknown, but maybe increased sebum production, or lipophilic yeast colonization (Malassezia furfur)
88
Treatment for seborrhea?
1. Dandruff shampoo: anti-proliferative, anti-fungal | 2. Topical corticosteroids if shampoo does not work
89
What are blistering diseases?
Diseases in which blisters are the primary and distinctive feature: 1. Pemphigus vulgaris 2. Bullous pemphigoid
90
In what conditions can blisters be seen? What to note?
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
Are blistering diseases common?
NOPE
92
Difference between desmosomes and hemidesmosomes?
Desmosomes connect cells to each other Hemidesmosomes are located at the basal surface and connect cells to the ECM
93
What is pemphigus?
Rare autoimmune blistering disorder with loss of desmosomes => vesicles and bullae that rupture easily upon touching (Nikolsky sign) => leave erosions in skin
94
Most common type of pemphigus?
Pemphigus vulgaris
95
Can pemphigus be life-threatening?
YUP
96
Treatment for pemphigus and bullous pemphigoid?
Systemic steroids or other immunosuppressives
97
Pathogenesis of pemphigus? What to note?
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
What is bullous pemphigoid?
Autoimmune bullous disorder forming tense blisters (2-8 cm) that do not rupture and can heal without scarring
99
Pathogenesis of bullous pemphigoid? What to note?
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
Immunofluorescence pattern of Pemphigus?
Fishnet/mesh
101
Immunofluorescence pattern of bullous pemphigoid?
Linear along the dermal-epidermal junction