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MABS Immunology > lecture 36 > Flashcards

lecture 36 Flashcards

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1
Q

a type I allergic response seen primarily in children

A

Atopic dermatitis

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2
Q

atopic dermatitis is what type of allergic response?

A

type I allergic response

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3
Q

itchy red skin that cannot retain moisture, lichenification, ichthyosis, atopic pleat.

A

Symptoms of atopic dermatitis

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4
Q

this disease is caused by a mutation of filaggrin + physical damage to skin allows allergens in, causing IgE/mast cell response.

A

Atopic dermatitis

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5
Q

a rare painful blistering autoimmune disease of skin

A

Pemphigus

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6
Q

this pemphigus is superficial (IgG4 autoantibody vs. desmoglein-1)

A

foliaceous

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7
Q

this pemphigus is deep (IgG4 autoantibody vs. desmoglein-3)

A

vulgaris

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8
Q

presence of acanthocytes

A

Nikolsky’s sign

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9
Q

smear help to diagnose pemphigus

A

Tzanck smear

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10
Q

chronic immune-mediated attack of endothelial cells, causing edema, fibrosis, atrophy. May also cause telangiectasia, calcinosis, flexion contractures, and digital ischemia-Raynaud’s phenomenon

A

Scleroderma

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11
Q

a multisystemic type III hypersensitivity/autoimmune disease that causes malar rash, alopecia and mucosal ulcers.

A

Lupus

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12
Q

these factors trigger lupus

A

Genetic and environmental factors

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13
Q

bimodal distribution for onset, is Th1, Th17 hyperproliferation response, and has 5 cardinal signs

A

Psoriasis

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14
Q

what are the five cardinal signs for psoriasis

A
  1. Red raised plaques 2. Well circumscribed margins 3. Bright salmon red color 4. Silvery micaceous scale 5. Symmetric distribution
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15
Q

a focal, segmental or generalized immune-mediated destruction of melanocytes mediated by NK cells, causing patchy lightened areas of skin and hair. No gender or ethnic predisposition

A

Vitiligo

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16
Q

Type I hypersensitivity response causing chronic skin inflammation

dry, intensely itchy skin + raised red rash and inability of skin to hold moisture

infants & children

A

atopic dermatitis

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17
Q

allergic response
underlying defect in epidermal barrier function(filiaggrin defect)
Stress and physical damage to the skin
Th2 and B cell response

A

Predisposition to development of Atopic Dermatitis

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18
Q 
soaps and detergents
cosmetics
clothing
sweat
allergens
stress
temperature changes
jewelry
A

causes of eczema

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19
Q 
itching
ichthyosis
keratosis pilaris
hyperlinear palms and cheilitis
atopic pleat
blisters ooze and crust
lichenification
A

symptoms of atopic dermatitis

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20
Q

the diagnosis and pathophysiology of AD can be easily determined from this method?

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A

a physical exam

21
Q

how to best treat AD?

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A

moisturizing with thick creams
corticosteroids
vitamin D
dilute bleach bath

22
Q

group of rare autoimmune blistering epithelial disorders that results from loss of normal intercellular attachments in epidermis

23
Q

autoimmune destruction of desmoglein 1 (in epidermis, esp scalp). Least severe form of pemphigus.

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A

Pemphigus foliaceus

24
Q

autoimmune destruction of desmoglein 3 lesions in epidermis & mucous membranes (e.g., in mouth) (basal layer of epidermis- 2ndary bacterial infections), more severePemphigus vulgaris (more severe)

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A

Pemphigus vulgaris (more severe)

25
``` Ashkenazi Jewish or Mediterranean descendants are at increased risk Genetic factors: MHC class II– DRB*0402,DQB1*0503 ``` predisposition for which disease?
pemphigus vulgaris
26
Painful flaccid, fragile bullae manifests as erosions/ulcers in the mouth Mortality rate 5-15% with corticosteroid therapy
Symptoms of pemphigus vulgaris
27
``` desmoglein free-floating keratinocytes (acanthocytes) Positive Nikolsky’s sign acantholytic cells tombstoning Direct immunofluorescent staining Tzanck smear ```
Diagnosis and Pathophysiology of PV
28
site of antibody attack in PV
Desmoglein-3
29
processed by APCs, presented to helper 2 T cells, which upregulate plasma cell production of IgG4
Desmoglein
30
``` Corticosteroids Methotrexate Immunosuppressants Rituximab Sulfasalazine, pentoxifylline Cyclophosphamide ```
Treatment of PV very difficult to control
31
produced on the surface of immature B cells and plays a role in plasma cell formation
CD20
32
Chronic immune-mediated fibrosis /vasculopathy of skin Fibroblasts deposit collagen and extracellular matrix in skin Females > males immune-mediated targeting of endothelial cell nuclei in blood vessels edema, perivascular cuffing, and fibroblast activation (scarring) Cytomegalovirus triggers autoimmunity Exposure to organic solvents Microchimerism (fetal antigens in maternal blood trigger immune response).
Predisposition to Scleroderma
33
First symptom: swollen fingers & hands +/- ulceration flexion contractures Blood vessels appear prominently (mottled color). Late stage – telangiectasia (mottled blood vessels), calcinosis, digital ischemia. Raynaud’s phenomenon
Symptoms of Scleroderma
34
``` Diagnosis: presence of antibodies Treatments: Symptomatic (NSAIDS, steroids, etc.) Calcium channel blockers for Raynaud’s. Chemotherapy – Bleomycin, taxane, methotrexate, or cyclosporine to treat the autoimmune component of the disease ```
Diagnosis and Treatments of Scleroderma
35
``` common in non-European women Chronic multisystem autoimmune disease Inflammation type III hypersensitivity reaction Genetic: mutations on chromosome 6 (RUNX-1) Environmental triggers: UV radiation Infectious agents (bacteria, viruses) Drugs (antidepressants, antibiotics) ```
Predisposition to Lupus
36
(malar rash), alopecia, mucosal ulcers
common symptoms of Lupus
37
``` Single gene mutations Combination of genes (penetrance/single nucleotide polymorphisms) Environmental triggers (Epstein Barr Virus) Toxic substances (smoking or heavy metal exposure) Abnormal immune response molecular mimicry, failure of inactivation by Tregs (CD4+FoxP3+CD25+) Random events (hormonal factors) ```
Triggers of autoimmunity for lupus
38
SLICC, 4+ criteria, at least 1 clinical, 1 lab
SLE Diagnostic Criteria
39
Avoid the sun, use sunscreen vs. UVA and UVB Topical corticosteroids for rashes NSAIDS and symptomatic treatments Antimalarials for joint and muscle pain
Treatment of Lupus
40
usually at puberty/menopause aggravated by environmental factors: Infections: group A strep, HIV infection Stress Alcohol and drugs: prednisone, beta blockers, lithium Strong MHC association: HLA-Cw602, HLA-DR7
Predisposition to Psoriasis
41
what are the main symptoms of psoriasis?
5 CARDINAL MORPHOLOGIC FEATURES 1. Red plaques (raised) 2. Well circumscribed margins 3. Bright salmon red color 4. Silvery micaceous scale (hyperproliferation) 5. Symmetric distribution (right and left) Koebner phenomenon
42
hyperproliferation damage incites an autoimmune response Th1- and Th17-mediated response, produces IFN-gamma, IL-2, and IL-22 to induce keratinocyte hyperproliferation
Diagnosis and Pathogenesis of Psoriasis
43
what are the keys in diagnosing psoriasis
1. Environmental trigger 2. Host DNA processed 3. Th1, Th17 response 4. IFN, TNF, IL-1, 2, 17, 22 5. Keratinocyte proliferation
44
Treatment of Psoriasis?
``` topical creams UVB or UVA + psoralens (PUVA) Systemic therapy: Methotrexate Acitretin (oral retinoid) Cyclosporine ```
45
Affects all races & genders equally early adulthood May run in families
Predisposition to Vitiligo
46
sun-exposed skin, body folds (e.g., armpits), prior sites of injury, around moles or body openings appears in one of three patterns: focal, segmental, generalized
Symptoms of Vitiligo
47
Physical exam Documented history of sun exposure (sunburn), rash, or skin trauma stress or illness
Diagnosis and Pathogenesis of Vitiligo
48
what is the pathogenesis of vitiligo?
Melanocyte destruction via antibody-mediated complement activation or ADCC Antibodies (IgG) are formed. NK cells have Fc receptor (called CD16). Ab binds to NK cell. This activates the NK cell. NK cell releases IFN gamma, And destroys the cell using perforin/granzyme.
49
``` No known way to prevent vitiligo Repigmentation treatments (long-term: 6-18 months): Cosmetics (to conceal depigmentation) UV light therapy Corticosteroid creams PUVA Autologous skin grafting Autologous melanocyte transplant Micropigmentation (tattooing) OR… depigmentation of unaffected skin areas ```
Treatment of Vitiligo

MABS Immunology (18 decks)

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