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Block 3 - Resp > Lecture 12 - Immune System In Cutaneous Diseases > Flashcards

Lecture 12 - Immune System In Cutaneous Diseases Flashcards

1
Q

Immunological cell behavior in skin

A
  • Langerhans cell sample the space for foreign antigens

- Dermal dendritic cells are migratory

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2
Q

Neutrophils and inflammation

A
  • participate in clearing of dead cells and pathogens
  • potentially amage tissue by releasing toxic mediators
  • release proinflammatory cytokines
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3
Q

4 types of cutaneous hypersensitivity

A
  • Type I: IgE mediated (anaphylaxis, urticaria)
  • Type II: Antibody-mediated (Bullous diseases)
  • Type III: Immune complex (Vasculitis)
  • Type IV: Cell mediated (CHS, DTH)
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4
Q

Type I hypersensitivity

A
  • anaphylaxis
  • urticaria
  • angioedema
  • things that make mast cells degranulate
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5
Q

Urticaria classification and types

A
  • Acute vs chronic (6 weeks +)
  • spontaneous vs induced
  • allergic (drug, infections, food)
  • contact (allergic)
  • physical (elicited by external stimuli: pressure, cold, heat, solar, vibrations)
  • cholinergic urticaria (elicited by increase in core body temp)
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6
Q

Acute urticaria

A
  • very common
  • post viral, particularly in children
  • various identifiable allergens
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7
Q

Direct mast cell degranulation can be caused by

A
  • Curare/ D- tubocurarine
  • opiates
  • radiocontrast
  • alcohol
  • ASpirin, NSAID
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8
Q

Chronic urticaria

A
  • spontaneous vs inducible
  • spontaneous: Due to known cause or due to unknown cause
  • Inducible: physical, cholinergic, contact, aquagenic
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9
Q

Prevalence of chronic spontaneous urticaria

A
  • 0.5-1%
  • Europe: 8 million
  • world: 80 million
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10
Q

Differential diagnosis of urticaria

A
  • erythema multiforme
  • urticarial vasculitis
  • urticaria pigmentosa
  • Rare syndromes
  • Eosinophilic cellulitis
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11
Q

Wheals
REcurret unexplained fever, joint pain, malaise
- autoinflammatory disease suspected

A
  • Acquired hereditary AID
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12
Q
  • wheals/angioedema
  • no fever, malaise or joint pain
  • average wheel druation more than 24 hours
  • signs of vasculitis in biopsy
A
  • urticarial vasculitis
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13
Q
  • no recurrent unexplained fever or joint pain or malase

- average wheal duration

A
  • chronic spontaneous urticaria
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14
Q
  • no recurrent unexplained fever or joint pain or malase

- average wheal duration

A
  • chronic inducible urticaria
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15
Q
  • Angioedema
  • ACE inhibitor treatment
  • remission after stop
A
  • ACE-Inh induced AE
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16
Q
  • Angioedema
  • no ACE inhibitor treatment
  • HAE or AAE suspected
A
  • HAE I-III AAE
17
Q

Ruling out severe inflammatory disease

A
  • ESR
  • CRP
  • differential blood count
18
Q

Causes of CSU

A
  • autoreactivity (20%)
  • infection (26%)
  • intolerance (38%)
  • other casues (2%)
  • unknown
19
Q

History for CSU

A
  • otherwise well?
  • recent travel?
  • pattern of urticaria?
  • how long do individual lesions last?
  • accompanying symptoms?
  • precipitating factors
20
Q

Investigation of CSU

A
  • FBC, ESR, differential
  • EUC, LFT, hepatitis serology
  • ANA
  • Hep B
  • Stool
  • biopsy
  • Food diary, dietary provocation test
  • prick testing not helpful
21
Q

Treatment of urticaria

A
  • avoid precipitating factors and direct mast cells degranulators
  • treat underlying abnormalities
22
Q

Symptomatic Urticaria therapy

A
  • second generation H1-Antihistamine (sgAH)
  • if symptoms persist after 2 weeks
  • Increase sgAH dose (up to 4 times)
  • If symptoms persist after 1-4 weels
  • add omalizumab, cyclosporine A or leukotriene antagonist
23
Q
  • olizumab
A
  • give an autoallergen to block IgE from binding Mast cells
24
Q

Type II/III hypersensitivity

A
  • antibody/antibody-complex mediated
  • organ speficic: thyrotoxicosis, pernicious anemia, Addison’s, goodpasture
  • Middle: pemphigus, pemphigoid, myasthenia gravis, ITP
  • Organ non-specific: Sjogrens, SLE, RA, sleroderma
25
Q

Pemphigus

A
  • Antibodies against intercellular cement susbtance: keratinocytes lose touch
  • intra-epidermal disruption: flaccid blisters and erosions
  • Mucous membrane involvement usually prominent (60% present with oral disease alone)
  • other mucosae
26
Q

Pemphigus group

A
  • vulgaris (anti-desmoglein 3 and 1 antibodies)
  • Foliaceus (anti-desmoglein 1 antibodies)
  • erythematosus
  • drug induced (Penicillamine, captopril)
  • paraneoplastic
  • pemphigus disrupts the desmosome
27
Q
  • Treatment of pemphigus
A
  • stop any causative drugs
  • oral corticosteroids
  • poisonsL steroid sparing drugs (Azathiprine, cyclophosphamide, methotrexate, cyclosporin)
  • IVIG
  • Plasmapheresis
  • Rituximab (anti-CD20)
28
Q

Other bullous disorders

A
  • pemphigus group
  • bullous pemphigoid and pemphigoid gestionis:
  • epidermolysis bullosa acquisita
  • linear IgA dermatosis
  • dermatitis herpetiformis
29
Q

Bullous pemphigoid

A
  • disrupts attachment to the basement membrane
  • very itchy disease
  • histology: subepidermal blister formation and an inflammatory infiltrate composed of neutrophils and eosinophils in the dermis and bukllla cavity
30
Q

Treatment of bullous pemphigoid

A
  • oral corticosteroids
  • poisons
  • IVIG
  • PLasmapheresis
  • Rituximab (anti-CD20)
31
Q

Type III hypersensitivity

A
  • allergic vasculitis
  • leukocytoclastic vasculitis
  • polyareteritis nodosa
  • usually in the legs
32
Q

Causes of small vessel vasculitis

A
  • Infection
  • Drugs (antibiotics)
  • autoimmune (SLE, RA, others…)
  • Malignancy: solid or lymphoproliferative)
  • idiopathic: LCCV (60%)
33
Q

Investigations in vasculitis

A
  • history
  • fever, nodes, spleen
  • investigate for cause/associations
  • investigate for extent: check the kidneys
34
Q

Treatment of vasculitis

A
  • remove antigen
  • rest, warmth, compression stokings
  • steroids
  • NSAIDs
  • Dapsone
  • Colchicine
  • immunosuppressants
35
Q

Type IV hypersensitivity

A
  • Contact hypersensitivity (epicutaneous Ag)
  • Delayed type hypersensitivity (intracutaneous Ag)
  • granulomatous hypersensitivity (leprosy)
36
Q

Treatment

A
  • identify antigen
  • remove antigen
  • steroids: topical, oral
37
Q

Atopic eczema

A
  • involves both humoral and cell-mediated immunity
  • IgE-mediated or T cell mediated allergies in many patients
  • CD4+ (Th2) mediated inflammation in skin
  • Skin barrier funciton disorder
38
Q

Atopic eczema

A
  • Type I: IgE mediated allergies
  • Type IV: house dust mite, pityrosporum yeasts, contact dermatitis to topical agents, staph toxins may act as superantigens

Block 3 - Resp (44 decks)

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