Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Allergy and Immunology > First Aid, Chapter 7 Hypersensitivity Disorders, Atopic Dermatitis (Eczema) > Flashcards

First Aid, Chapter 7 Hypersensitivity Disorders, Atopic Dermatitis (Eczema) Flashcards

1
Q

What should be considered in new onset dermatitis in an adult?

A

In an adult patient presenting with newonset dermatitis and no history of childhood eczema, asthma, or allergic rhinitis, the physician should consider other causes, such as cutaneous Tcell lymphoma (CTCL), which may require a skin biopsy for diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In atopic dermatitis, what causes a Th2 bias?

A

Environmental and bacterial stimuli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the prevalence of atopic dermatitis?

A

8-18%, and is increasing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What percentage of atopic dermatitis patients will develop asthma?

A

more than 50%, and even higher will have allergies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What type of cells are increased in both active AD and asthma, but not inactive disease?

A

FcER1-expressing IgE+ Langerhans cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What toxin is IgE present against in AD? and what forms of AD is it present in?

A

IgE to Staphylococcus aureus toxins is produced in both extrinsic and intrinsic forms of AD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which cells upregulate surface IgE to catch allergens that have infiltrated injured skin in AD?

A

Two distinct Ag-presenting dendritic cells in atopic skin, Langerhans cells and inflammatory dendritic epidermal cells (IDECs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which chemokines are specific for AD, increasing with acute symptoms and decreasing with improvement?

A

Cutaneous T–lymphocyte-attracting chemokine (CTACK and CCL27) and thymus and activatation-regulated chemokine (TARC) levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens to Tregs with superantigen stimulation in atopic dermatitis?

A

Superantigen stimulation causes CD4+CD25+ Treg cells to lose their immune suppressive activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What explains the susceptibility of AD skin to bacterial, viral, and fungal infections?

A

A decrease or absence of antimicrobial peptides, human β defensins (hBD-2 and hBD-3) and human cathelicidin (LL-37) in keratinocytes place patients at risk for infections with bacteria, fungi, and viruses. Deficiency in hBD-3 expression results in impaired killing of S. aureus. Downregulation of antimicrobial genes, due to local upregulation of Th2 cytokines, could explain the susceptibility of atopic dermatitis skin to bacterial, viral, and fungal infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What gene polymorphism is linked to severe AD w/ frequent bacterial infections?

A

A TLR2-gene polymorphism that results in an impaired TLR2 expression has been linked to severe AD with frequent bacterial infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a TLR2-gene polymorphism that results in impaired TLR2 expression associated with?

A

Severe AD with frequent bacterial infections.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is fillagrin? What are loss of function variants of fillagrin associated with?

A

It is an epidermal barrier protein. Loss of function variants of filaggrin can predispose patients to have earlier onset, more severe, and persistent AD. Loss-of-function mutations in filaggrin (FLG) are associated with increased risk for asthma when it occurs with atopic dermatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is expressed by keratinocytes in both acute and chronic lesions of AD?

A

TSLP (thymic stromal lymphopoietin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is TSLP? Where is it expressed?

A

TSLP (thymic stromal lymphopoietin) is expressed by keratinocytes in both acute and chronic lesions of atopic dermatitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What cells are involved in atopic dermatitis?

A

T lymphocytes, Langerhans cells, Inflammatory Dendritic Epidermal Cells (IDECs), and eosinophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What types of T lymphocytes are involved in atopic dermatitis? What do they express? What do the memory T cells express?

A

Predominantly CD3, CD4, CD45RO memory T lymphocytes that also express CD25 and human leukocyte antigen (HLA) DR on their surface. Most memory T lymphocytes express high levels of the homing receptor cutaneous lymphocyte-associated antigen (CLA), a ligand for vascular adhesion molecule, E selectin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do the Langerhans cells in atopic dermatitis express? What do they contain?

A

Express FcRI that bind IgE. FcRI on Langerhans cells lack the classic β chain. Langerhans cells contain Birbeck granules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the role of Inflammatory dendritic epidermal cells (IDECs) in atopic dermatitis?

A

FcRI-activated IDECs stimulate naïve T lymphocytes to become IFNγ-producing T lymphocytes. In combination with IL-12 and IL-18, this leads to switch from Th1 to Th2. IDECs do not contain Birbeck granules.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In what types of lesions are eosinophils found in atopic dermatitis? What type of lesions are they found in higher numbers? What protein is elevated and correlates with disease severity?

A

Activated eosinophils are present in significantly greater numbers in chronic than in acute lesions. Deposition of eosinophil, a major basic protein, can be detected throughout the dermis of involved areas. Serum levels of eosinophil cationic protein are elevated and correlate with disease severity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the FcER1 of Langerhans cells lack?

A

the beta classic beta chain. Mnemonic

You beta remember that the FcRI of Langerhans cells lack the classic beta chain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the cytokines involved in acute and chronic atopic dermatitis?

A

Acute: IL-4, IL-13:“4 Suits with 13 cards each in a deck, including the aces.” Chronic: IL-5, IL-12, IFNγ: “Education is chronic starting at 5 through Grade 12.”
Mnemonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which cell type expresses higher levels of FcERI: Langerhans cells or IDECs?

A

IDECs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is filaggrin expressed? A. Anterior vestibulum of nose B. Transitional nasal epithelium C. Respiratory nasal epithelium D. Human bronchial epithelium

A

A. Anterior vestibulum of nose

25
Q

How is extrinsic (atopic) eczema different than instrinsic (nonatopic) eczema when it comes to IgE, eosinophils, Il-4 and IL-13 production, and IL-10?
What percentage does extrinsic vs. intrinsic account for?

A 
Atopic: 
\+IgE mediated sensitization
\+eosinophilia
\+increased production of IL-4 and IL-13, causes increased IL-5 production.
IL-10 plays immune-modulating role

Nonatopic
No IgE mediated sensitization, +eosinophilia, Less production of IL-4 and IL-13, IL-10 plays immune-modulating role.

26
Q

What is the distribution of atopic dermatitis?

A
  • Involvement of face and extensor surfaces of extremities occurs in children younger than 2 years old.
  • Flexural involvement occurs in children older than 2 years of age and in adults.
27
Q

Which cytokine is primarily associated with pruritus in atopic dermatitis?

A

IL-31

28
Q

What are anterior cataracts associated with? What are posterior cataracts associated with?

A

Anterior cataracts are associated with atopic keratoconjunctivitis. Posterior cataracts are associated with Prednisone.

29
Q

What organism are associated with infection in atopic dermatitis?

A

AD is accompanied by an increased susceptibility to infections or colonization with a variety of organisms: S. aureus, herpes simplex, molluscum contagiosum, Pityrosporum orbiculare (formerly known as Malassezia furfur), and Pityrosporum ovale.

30
Q

How does atopic keratoconjunctivitis present?

A

AKC presents with bilateral intense ocular pruritus, burning, tearing, and copious mucoid discharge.

31
Q

What is an exam finding that may be seen in atopic keratoconjunctivitis?

A

horner-trantas dots

32
Q

Why mechanism causes visual loss in atopic keratoconjunctivitis?

A

corneal scarring

33
Q

Does atopic keratoconjunctivitis eye activity parallel skin involvement?

A

yes

34
Q

What conditions can complicate atopic keratoconjunctivitis of the eye?

A

Can be complicated by herpes infection, keratoconus (noninflammatory thinning of cornea), and anterior subcapsular cataracts.

35
Q

What aggravates hand dermatitis?

A

Wetting, especially in the work environment, can lead to occupational disability.

36
Q

What is eczema vaccinatum?

A

A rare, severe reaction to smallpox vaccination in patients with history of AD

37
Q

What percentage of atopic dermatitis patients might food allergens trigger flares in?

A

Double-blind, placebo-controlled food challenges have demonstrated that food allergens can trigger flares in some AD patients (e.g., 25–33% of those with moderate to severe disease).

38
Q

What are the main food culprits in atopic dermatitis?

A

Seven foods (milk, egg, soy, wheat, fish, peanuts, and tree nuts) account for nearly 90% of positive challenges.

39
Q

How does food elimination affect skin disease in AD?

A

Elimination of the causative food allergens results in the improvement of skin disease and a decrease in spontaneous basophil histamine release.

40
Q

Can aeroallergens trigger AD? Based on what evidence?

A

Evidence supporting a role for aeroallergens includes finding of both allergen-specific IgE antibodies and antigen-specific T lymphocytes. Environmental control measures, such as dust mite avoidance, resulted in clinical improvement in AD.

41
Q

What role do autoantigens play in AD? By what mechanism?

A

Sera from some patients with severe AD have been found to have IgE antibodies directed against human protein. The release of allergens against self from damaged tissues triggers IgE- or T–lymphocyte-mediated responses and maintains chronic allergic inflammation in severe AD.

42
Q

What are patients with AD colonized with? What role do superantigens play in triggering AD?

A

Patients with AD are colonized with high numbers of S. aureus. Exotoxins secreted by S. aureus can act as superantigens, contributing to persistent inflammation or inflammation of AD.

43
Q

What is increased colonization associated with in AD as far as molecules?

A

Increased colonization may be associated with decreased antimicrobial peptides, H-B defensin (HBD-2 and 3), and human cathelicidin (LL-37) by keratinocytes.

44
Q

What is the role of IgE to toxins in AD?

A

AD patients can make specific IgE antibodies against the toxins on their skin, and their disease severity appears to correlate with the presence of these antibodies.

45
Q

Deficiency of which antimicrobial peptide in atopic skin may contribute to eczema vaccinatum?

A

LL-37

46
Q

What are the general categories of skin disorders that is in the differential of atopic dermatitis?

A

Chronic dermatoses, infections and infestations, malignancy, immune deficiencies, metabolic disorders, and proliferative disorders

47
Q

What is Netherton syndrome?

A

Congenitally acquired scaly dermatitis with short, spiky, brittle hair, called “bamboo hair

48
Q

What is seborrheic dermatitis?

A

Greasy, scaly rash with well-defined edges in areas with sebaceous glands (i.e., scalp, face, and periauricular)

49
Q

What is nummular eczema?

A

Clearly demarcated edge Lesions on limbs more so than on trunk Variable intermittent course

50
Q

What is lichen simplex chronicus?

A

Cutaneous response to repeated rubbing or scratching Common in neck or fold behind ear (areas commonly reached) Accentuation of surface marking (e.g., resembles tree bark)

51
Q

Describe scabies infection.

A

Eczematous vesicles on hands and feet Pityriasis that is rosea-like

52
Q

What immune deficiencies might you consider in AD?

A

-Wiskott-Aldrich syndrome (WAS): Child with dermatitis, low platelets, and recurrent infection
-Severe combined immunodeficiency (SCID)
Dermatitis: failure to thrive, diarrhea, and lifethreatening infections
-Hyper-IgE syndrome: Chronic eczema with impetigo
-IPEXa syndrome: Infant with dermatitis, intractable diarrhea, diabetes, and hypothyroid FOXP3 mutation
-Dock8 deficiency: Respiratory tract infections, difficult to treat viral skin infections (HPV-associated warts, orolabial/anogenital/corneal HSV, molluscum, severe varicella or herpes zoster), bacterial skin infections and/or mucocutaneous candidiasis. High incidence of malignancy

53
Q

What metabolic disorders are on the differential of AD? Describe them.

A
  • Zinc deficiency; acrodermatitis enteropathica: Infant with eczema that does not respond to steroids Periorificial rash Necrotic areas around nose
  • Pyridoxine (vitamin B6 and niacin deficiency): Seizures, irritability, and cheilitis
  • Multiple carboxylase deficiency: Infant with skin rash, alopecia, and lethargy
  • Phenylketonuria: Pale pigmentation, blue eyes, and scleroderma If untreated, leads to mental retardation
54
Q

What proliferative disorder is on the differential of AD? Describe it.

A

Letterer-Siwe disease- Infants with anemia, thrombocytopenia, lymphadenopathy, and histiocytic infiltration of liver, spleen, and lymph nodes

55
Q

What infections might be treated/prevented with antibiotics, antivirals, and antifungals in AD?

A

Helpful in reducing secondary infections that can complicate AD such as S. aureus, herpes simplex, P. ovale, Candida, or scabies

56
Q

What is the role of vitamin D in AD?

A

Has been shown to enhance innate immune responses in patients with AD. Especially helpful in patients with house dust mite sensitization o

57
Q

A 3-year-old boy presents to the pediatrician with bloody stools, draining ears, and eczema. What primary immunodeficiency should be considered?

A

Wiskott-Aldrich syndrome

58
Q

Oral vitamin D induces production of which antimicrobial peptide in atopic individuals?

A

Cathelicidin

Allergy and Immunology (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions