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BMS250 > Dermatology Part 4: Pathophysiology of Dermatitis (Week 3) > Flashcards

Dermatology Part 4: Pathophysiology of Dermatitis (Week 3) Flashcards

1
Q

What is atopic dermatitis also known as?

A

Atopic eczema or AD

Atopic dermatitis is a chronic inflammatory and complex familial transmitted skin disease. It usually begins in childhood with a variable natural course.

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2
Q

What are the hallmark symptoms of atopic dermatitis?

A

Itch

Itch is often unrelenting in severe cases, leading to sleep disturbance and excoriated, infection-prone skin.

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3
Q

What is the prevalence peak of atopic dermatitis in early childhood in industrialized countries?

A

15% to 20%

Atopic dermatitis has variable rates of remission, with many patients experiencing symptoms into adulthood.

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4
Q

What are the major features of atopic dermatitis?

A
  • Pruritus
  • Eczematous dermatitis (acute, subacute, or chronic)
  • Facial, scalp, and extensor involvement in infancy
  • Flexural eczema or lichenification in children and adults
AD in infancy

Note: the diaper area is usually spared in infants

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5
Q

What is commonly associated with atopic dermatitis?

A
  • Personal or family history of atopy (see footnote)
  • xerosis (dry skin) or skin barrier dysfunction
  • Immunoglobulin E reactivity

Atopy includes allergic rhinitis, asthma, and atopic dermatitis.

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6
Q

What are the primary factors driving the pathogenesis of atopic dermatitis?

A
  • Skin barrier defects (FLG gene)
  • Environmental effects
  • Alterations in immunologic responses (e.g., in T cells, antigen processing, allergen sensitivity, infection, etc.)
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7
Q

What is the prevalence of atopic dermatitis in adults in industrialized countries (e.g, US, Germany, Japan)?

A

3–7%

The condition has tripled in prevalence since the 1960s.

Note that the female:male ratio is ~ 1.3:1 (thus slightly more common in females)

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8
Q

What are the characteristics of acute lesions in atopic dermatitis?

A
  • Appearance: Erythematous papulovesicles (small red bumps or blisters)
    *Surface Changes: Pinpoint crusting or frank weeping
    *Symptoms: Highly pruritic
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9
Q

How do subacute or chronic lesions of atopic dermatitis typically present?

A
  • Appearance: Dry, scaly plaques
  • Surface Changes: Excoriation (from scratching) and lichenification
    *Symptoms: Persistent pruritus, with less erythema (compared to acute lesions)

Note: Lesions can present with a single stage of lesions (e.g., acute OR chronic) or a mixture of acute AND chronic lesions

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10
Q

In patients with darker skin tones, what are some clinical features of atopic dermatitis?

A
  • Follicular accentuation
  • Flat-topped papules in lichenified areas
  • Tendency toward hyperpigmentation

Rarely, patients may experience a vitiligo-like depigmentation

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11
Q

What is the primary manifestation of atopic dermatitis in many adults?

A

Chronic hand eczema

At least one third of patients will show clinical features of filaggrin deficiency (e.g., ichthyosis vulgaris, keratosis pilaris, and hyperlinear palms)

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12
Q

What complications are associated with atopic dermatitis?

A
  • Bacterial infections
  • Viral infections
  • Fungal infections
  • Ocular issues (e.g., eyelid dermatitis)
  • Hand dermatitis
  • Exfoliative dermatitis (e.g., may involve general redness, scaling, weeping, crusting, systemic toxicity, lymphadenopathy, and fever; rare but can be life threatening)
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13
Q

What factors contribute to decreased skin barrier function in atopic dermatitis?

A
  • Downregulation of cornified envelope genes (e.g., keratin, filaggrin, loricrin)
  • Reduced ceramide levels
  • Increased proteolytic enzyme activity
  • Enhanced transepidermal water loss (TEWL)
  • Addition of soap and detergents to the skin can raise skin pH, making it more alkaline, and increase activity of endogenous proteases (leading to further breakdown of epidermal barrier function)
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14
Q

What is the role of filaggrin in atopic dermatitis?

A

Impaired skin barrier function

Filaggrin gene mutations can lead to increased transepidermal water loss and allergen entry.

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15
Q

What is the immune response characterized by in atopic dermatitis?

A

T helper 2 (Th2) immune activation

This includes high levels of IgE and eosinophilia.

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16
Q

What cytokines are predominantly expressed in nonlesional and acute atopic dermatitis lesions?

A
  • IL-4
  • IL-5
  • IL-13
  • IL-25
  • IL-31
  • IL-33
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17
Q

True or False: Neutrophils are commonly found in atopic dermatitis skin lesions.

A

False

Neutrophils are absent even with increased Staphylococcus aureus colonization.

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18
Q

What is the significance of thymic stromal lymphopoietin (TSLP) in atopic dermatitis?

A

Activates dendritic cells promoting Th2 immune responses

TSLP is highly expressed in AD skin.

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19
Q

What key difference exists between nonlesional and lesional atopic dermatitis skin?

A

Dendritic cells exhibit fewer surface-bound IgE molecules in nonlesional skin.

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20
Q

What is the role of IL-23 in atopic dermatitis?

A

Enhances IL-22–IL-17 differentiation

IL-4 and IL-13 can further enhance IL-23 production by dendritic cells (Note: blockade of these may be therapeutic targets)

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21
Q

What are the effects of reduced epidermal differentiation in atopic dermatitis?

A
  • Decreased production of epidermal structural proteins
  • Decreased production of antimicrobial peptides
  • Impaired filaggrin production
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22
Q

What are the effects of reduced epidermal differentiation?

A

Decreased production of:
* Epidermal structural proteins
* Filaggrin breakdown products
* Epidermal lipids
* Antimicrobial peptides (AMPs)

Reduced epidermal differentiation impacts the skin’s barrier function and overall health.

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23
Q

Which cytokines are key in downregulating filaggrin expression?

A

TSLP, IL-4, and IL-13

These cytokines are potent inhibitors of filaggrin production in keratinocytes.

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24
Q

Which cytokines act synergistically with IL-4 and IL-13?

A

IL-17, IL-22, IL-25, and IL-33

These cytokines further suppress epidermal protein and lipid expression.

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25
Q

What contributes to the enhanced allergen and microbial penetration in atopic dermatitis (AD)?

A

Defective epidermal barrier function, altered epidermal acidification, and loss of moisturization

These factors lead to an increased immune response and clinical manifestations of AD.

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26
Q

What is pruritus and its significance in atopic dermatitis?

A

Pruritus is a prominent feature of AD, leading to cutaneous hyper-reactivity and scratching

Control of pruritus is critical to prevent the vicious scratch–itch cycle that exacerbates AD.

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27
Q

True or False: H1 antihistamines are effective in controlling the itch of atopic dermatitis.

A

False

Allergen-induced release of histamine is not the sole cause of pruritus in AD.

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28
Q

Which cytokine is key in pruritus and released by activated T cells?

A

IL-31

IL-31 acts directly on sensory nerves to induce itching.

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29
Q

Name two stress-induced neuropeptides that amplify the itch response.

A

Substance P and CGRP (calcitonin gene-related peptide)

These neuropeptides sensitize nerve endings in the skin.

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30
Q

What is allergic contact dermatitis (ACD)?

A

A cell-mediated hypersensitivity reaction: Type IV (delayed-type) hypersensitivity

ACD is triggered by skin contact with environmental allergens.

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31
Q

What is the hallmark clinical presentation of ACD?

A

Eczematous dermatitis characterized by redness, itching, swelling, and vesicle formation

Chronic exposure can lead to lichenification and scaling.

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32
Q

What is the role of haptens in allergic contact dermatitis?

A

Haptens bind to skin proteins to form complexes that are recognized as foreign

This sensitization leads to T cell activation and an inflammatory response.

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33
Q

What is the diagnostic gold standard for identifying causal allergens in ACD?

A

Patch testing

Recommended for patients with persistent or recurrent dermatitis when ACD is suspected.

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34
Q

True or False: Irritant dermatitis requires complete avoidance of irritants to resolve.

A

False

Decreasing the duration and frequency of contact with irritants may improve symptoms.

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35
Q

What are the key symptoms of allergic contact dermatitis?

A

Itch and swelling

These symptoms provide clues to an allergic etiology.

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36
Q

What is the primary mechanism of allergic contact dermatitis?

A

Type IV hypersensitivity reaction triggered by exposure to an environmental allergen

Requires prior sensitization to develop a response.

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37
Q

What are the stages of dermatitis in allergic contact dermatitis?

A

Sensitization phase and elicitation phase

The sensitization phase lasts 10–15 days and is typically asymptomatic.

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38
Q

What is the role of Langerhans cells in allergic contact dermatitis?

A

Uptake hapten-protein complexes and present them to naïve T cells

This activates T cells and leads to the development of memory T cells.

39
Q

What does the acute phase of allergic contact dermatitis typically present with?

A

Pruritus, erythema, edema, and vesicles

Symptoms are usually confined to the area of direct exposure.

40
Q

What factors influence the expression of irritant dermatitis?

A

Climate and season, occlusion, frequency, and concentration of the irritant

These factors can exacerbate the condition.

41
Q

What histological appearance is associated with dermatitis?

A

Spongiosis

This appearance indicates an inflammatory disruption of the epidermis.

42
Q

What happens during the epidermal insult phase of irritant dermatitis?

A

Barrier function of the epidermis is diminished by irritants

This leads to damage to keratinocytes and recruitment of inflammatory cells.

43
Q

What is a common misconception about allergic contact dermatitis?

A

ACD is not always bilateral even with bilateral antigen exposure

Eczematous manifestations can be patchy despite uniform exposure.

44
Q

What is the relationship between irritant dermatitis and allergic dermatitis?

A

Irritant dermatitis predisposes to allergic dermatitis

Innate immune signals from irritant dermatitis can trigger allergic responses.

45
Q

What role does irritant dermatitis play in allergic contact dermatitis?

A

Irritant dermatitis predisposes to allergic sensitization to antigens that would not normally cause allergic contact dermatitis on non-inflamed skin.

46
Q

What is the relationship between potent sensitizers and irritant properties?

A

Potent sensitizers that can cause allergy on previously non-inflamed skin are dependent on their inherent irritant properties.

47
Q

What response do athymic mice exhibit when sensitized with oxazolone?

A

Athymic mice mount a neutrophil response and some diminished T-helper (Th)1/Th2 cell response to the sensitizer oxazolone.

48
Q

How do FcγR knockout mice respond to sensitization and rechallenge with oxazolone?

A

FcγR knockout mice have a greatly diminished response when sensitized and rechallenged with oxazolone.

49
Q

What is seborrheic dermatitis?

A

Seborrheic dermatitis is a common inflammatory skin disease affecting various age groups.

50
Q

What are the clinical features of seborrheic dermatitis?

A

Erythematous, greasy, scaling patches and plaques appear on scalp, face, ears, chest, and intertriginous areas.

51
Q

What age groups are commonly affected by seborrheic dermatitis?

A

Common in adolescents and young adults, with higher incidence in individuals older than 50 years.

52
Q

What is the prevalence of seborrheic dermatitis in the general population?

A

Varies between 2.35% and 11.30% depending on the study.

53
Q

What demographic trend is observed in seborrheic dermatitis?

A

Male predominance observed across all ages.

54
Q

What seasonal factors can affect seborrheic dermatitis?

A

Cold and dry climates exacerbate SD; sun exposure may reduce severity.

55
Q

What are the multifactorial causes associated with seborrheic dermatitis?

A

Several endogenous and exogenous predisposing factors are associated with SD.

56
Q

What is the significance of sebaceous glands in seborrheic dermatitis?

A

The role of sebaceous glands is notable considering time and lesional distribution of SD.

57
Q

What underlying diseases are associated with a higher prevalence of seborrheic dermatitis?

A

More common in individuals with certain underlying diseases such as AIDS and Parkinson disease.

58
Q

What is the role of the immune system in seborrheic dermatitis?

A

SD is more common in immunosuppressed patients, suggesting an important immune component in its pathogenesis.

59
Q

What findings were observed in DBA/2 2C TCR transgenic mice regarding seborrheic dermatitis?

A

Exhibited SD-like eruptions, supporting the role of T cells in SD.

60
Q

What changes in T-cell populations were reported in seborrheic dermatitis patients?

A

Decreased CD4+-to-CD8+ ratio, increased CD8+ cells, and increased production of immunoglobulin A and G antibodies.

61
Q

What inflammatory cytokines are increased in seborrheic dermatitis lesions?

A

IL-1α, IL-1β, IL-4, IL-12, tumor necrosis factor-α, and interferon (IFN)-γ.

62
Q

What is the significance of Malassezia in seborrheic dermatitis?

A

Malassezia is suggested to play an important role in SD pathogenesis.

63
Q

Which Malassezia species are most significant in seborrheic dermatitis?

A

Malassezia globosa and Malassezia restricta.

64
Q

What role do lipase and phospholipase enzymes play in Malassezia’s virulence?

A

They contribute to invasion of skin layers and dissemination across affected areas.

65
Q

What is the pathogenic effect of Malassezia furfur in seborrheic dermatitis?

A

Disrupts the protective skin barrier and induces inflammation.

66
Q

What is the role of oleic acid in seborrheic dermatitis?

A

Can cause dandruff-like flaking in susceptible individuals.

67
Q

What is the relationship between epidermal barrier disruption and seborrheic dermatitis?

A

Susceptibility is linked to a disrupted epidermal barrier, allowing penetration of irritating metabolites.

68
Q

What does the increased epidermal turnover in seborrheic dermatitis implicate?

A

Implies SD is a disorder of hyperproliferation.

69
Q

What treatments have been successful in seborrheic dermatitis when amphotericin B failed?

A

Keratolytics and anti-inflammatory medications.

70
Q

Fill in the blank: The increase in activity of _____ may explain the basis of using cytostatic medications in seborrheic dermatitis.

A

calmodulin

71
Q

True or False: Patients with atopic dermatitis often have atopic comorbidities, such as allergic asthma dn allergic rhinitis

A

True

This can impair quality of life

72
Q

True or False: AD is usually acute and located in extensor surfaces on infants and chronic and located in flexural surfaces on older children

A

True

Sites affected in older children are more similar to the adult presentation

73
Q

True or False: People who suffer from AD often show comorbid signs of T helper 2 (Th2) immune activation

This includes high levels of total and specific serum IgE, eosinophilia, and a predisposition toward allergic comorbidities

A

True

74
Q

Reduced expression of cornified envelope genes (e.g., keratin, filaggrin, and loricrin) weakens what layer of the epidermis?

A

stratum corneum

Thereby increasing vulnerability to allergens, irritants and pathogens

75
Q

What can further worsen epidermal barrier damage in AD?

A
  • scratching
  • exposure to EXOGENOUS proteases from house dust mites and S. aureus

Note: This is worsened by the lack of certain ENDOGENOUS protease inhibitors in atopic skin

Note: These epidermal changes likely contribute to INCREASED allergen absorption & microbial colonization

76
Q

What chromosome is the filaggrin gene found on?

A

chromosome 1q21

This chromosome contains other genes that are all involved in the epidermal differentiation complex (EDC)

77
Q

Mutations can impair skin barrier function. Impaired barrier leads to…

A
  • increased transepidermal water loss (TEWL)
  • increased attachment and entry of allergens and chemicals
  • inflammatory skin responses
78
Q

How can we characterize AD based on clinical appearance and duration?

A
  • non-lesional AD
  • acute AD lesions (3 or fewer days after onset)
  • chronic skin lesions (>3 days’ duration)
79
Q
  • mild epidermal hyperplasia (thickening of epidermis)
  • sparse perivascular T-cell infiltrate in the dermis
  • not entirely “normal”

Is this characteristic of non-lesional AD, acute AD lesions, or chronic skin lesions?

A

non-lesional AD

80
Q
  • Epidermal spongiosis: Intercellular edema in the epidermis, leading to disruption of keratinocyte cohesion
  • T-Cell Activation: Increased infiltration of activated memory T-cells with skin-homing cutaneous lymphocyte-associated antigen (CLA).

Is this characteristic of non-lesional AD, acute AD lesions, or chronic skin lesions?

A

acute AD lesions

Other Immune Cells:
- Rare presence of eosinophils, basophils, and neutrophils.
- Mast cells: Found in various stages of degranulation, contributing to inflammation and itch.

81
Q
  • Hyperplastic epidermis with elongation of rete ridges
  • Prominent hyperkeratosis (thickened keratin layer)
  • Minimal spongiosis (reduced intercellular edema)

Is this characteristic of non-lesional AD, acute AD lesions, or chronic AD skin lesions?

A

chronic AD skin lesions

82
Q

Commonality between non-lesional and lesional AD skin

A

Dendritic antigen-presenting cells:

  • Langerhans cells (LCs)
  • Inflammatory dendritic epidermal cells (IDECs) - Macrophages
83
Q

Key difference between non-lesional and lesional AD skin

A

In nonlesional AD, dendritic cells exhibit fewer surface-bound immunoglobulin E (IgE) molecules, compared to lesional AD skin

84
Q

Immune cell characteristics in chronic AD

A
  • Increased IgE-bearing Langerhans cells (LCs) in the epidermis
  • Macrophages dominate the dermal mononuclear cell infiltrate
  • Increased mast cells, but fully granulated (non-degranulated)
  • Neutrophils: Absent in AD skin lesions, even with increased Staphylococcus aureus colonization or infection
  • Eosinophils: Increased in chronic AD skin lesions
85
Q

Key differences between AD epidermis vs. normal epidermis

A

In AD epidermis…

1) Thymic Stromal Lymphopoietin (TSLP):
- Highly expressed in AD skin
- Activates dendritic cells, which promote Th2 immune responses, enhancing inflammation

2) Interleukin-33 (IL-33):
- Released by damaged or stressed keratinocytes
- Potentiates type 2 immunity, amplifying allergic inflammation

Note: type 1 and type 2 immunity = subsets of adaptive immune system

type 1 = Th1-driven, focused on intracellular pathogens (viruses, some bacteria).

type 2 = Th2-driven, focused on extracellular pathogens (helminths, allergens)

86
Q

True or False: AD keratinocytes lack significant levels of TSLP and IL-33, highlighting their role as key drivers of AD inflammation.

A

False

NORMAL keratinocytes lack significant levels of TSLP and IL-33, highlighting their role as key drivers of AD inflammation.

87
Q

True or False: With respect to treatment strategy, targeting specific cells is more effective than targeting cytokines in managing atopic dermatitis (AD)

A

False

Cytokine targeting is more effective than targeting specific cells in managing atopic dermatitis (AD).

Note: in particular, we want to target type 2 cytokines

88
Q

What are the key functions of type 2 cytokines?

A

In animal models, they replicate clinical features of AD, including:
- Elevated IgE responses
- Eosinophilia.
- Skin barrier dysfunction
- Allergic skin inflammation
- Itching

89
Q

Other cytokine pathways, including IL-22-IL-17 (along with IL-4 and IL-13) also play a significant role in AD and can inhibit:

A
  • terminal keratinocyte differentiation
  • filaggrin expression, contributing to skin barrier dysfunction
90
Q

What changes during the transition from acute to chronic AD?

A
  • increased Th1 cytokines
  • elevated IL-5

Both of these contribute to more inflammation

91
Q

True or False: TSLP can be detected in at-risk infants before AD onset

A

True

92
Q

Which chemokines are invovled in AD?

A
  • CTACK (aka CCL27)
  • CCR4
  • MDC (aka CCL22)
  • TARC (aka CCL17)

These help recruit T cells to inflamed skin

93
Q

Which chemokine is most associated with AD severity?

A

thymus and activation-regulated cytokine (TARC; aka CCL17)

94
Q
A

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