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Hypersensitivity Flashcards

1
Q

Type I hypersensitivity immune reactant

A

IgE

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2
Q

Hypersensitivity

A

An excessive immune response against foreign, often innocuous, antigens - which may result in tissue damage or death

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3
Q

Sensitization

A

The initial exposure to an antigen that primes the immune system to elicit a reaction to a subsequent exposure to that antigen

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4
Q

Allergen

A

Antigen that elicits immediate hypersensitivity

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5
Q

Allergy

A

A reaction caused by an allergen

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6
Q

Atopy

A

Familial predisposition (genetic) reaction to allergen

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7
Q

Cells involved in type I hypersensitivity

A

Mast cells, basophils, and eosinophils

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8
Q

Histamine

A

An amine derivative of histidine that is involved in vasodilation and increase capillary permeability

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9
Q

Where is histamine released from?

A

Exosomes; means immediate result (no transcription/translation)

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10
Q

What do mast cells and basophils release to mediate type I hypersensitivity reaction?

A
  • Histamines
  • Lipid mediators: Leukotrines and prostaglandins
  • Cytokines
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11
Q

Leukotrienes function

A

Smooth muscle contraction, increase capillary permeability, and mucus secretion

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12
Q

Prostaglandins function

A

Vasodilation and increase capillary permeability, PMN recruitment

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13
Q

Cytokines involved in type I hypersensitivity with mast cells/basophils and their functions

A

TNF-alpha: proinflammatory cytokine

IL-4, IL-5, IL-13: Th2 response

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14
Q

Sensitization response

A
  1. ) Prior to the hypersensitivity reaction, the individuals must have been exposed to the allergen
  2. ) Prototypical immune response for adaptive immunology takes place
  3. ) Production of plasma cells that secrete allergen-recognizing IgE
  4. ) IgE associates with the Fc receptor (FcεRI) on mast cells and primes, or sensitizes it for quick activation
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15
Q

2 phases of immediate reaction

A

Effector or elicitation phase and late-phase reaction

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16
Q

Effector/elicitation phase in immediate reaction

A
  1. ) Exposure to the antigen again is immediately recognized by the IgE-bound antibody on mast cells (crosslinking of the FcεRI receptors activate mast cells)
  2. ) Activation of mast cells result in degranulation and release of mediators (the vasoactive amines and lipid mediators result in the immediate reaction)
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17
Q

Late-phase reaction in immediate reaction

A
  • Cytokines result in this a few hours after exposure
  • Few hours post exposure
  • Accumulation of PMNs, eosinophils, basophils, T helper cells, and their mediators
  • May occur without prominent immediate reaction
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18
Q

Immediate reaction in immediate hypersensitivity

A
  • Seconds to minute exposure
  • Histamine and lipid mediators increase vascular permeability
  • Wheal-and-flare response
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19
Q

Wheal

A

Redness and local swelling due to initial vessel dilation

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20
Q

Flare

A

Subsequent dilation promotes red rim

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21
Q

Chronic allergic inflammation

A

repeated exposure that results in persistent inflammation – may alter tissue (asthma, eczema, hay fever)

22
Q

Immediate hypersensitivity anaphylaxis

A

Systemic activation of mast cells (such as from a bee sting) can lead to severe anaphylaxis

23
Q

Anaphylaxis leads to…

A

Widespread vascular permeability and fluid leaving blood, may cause BP to drop

24
Q

Clinical features of anaphylaxis

A

Resp: nasal obstruction, increased mucus, dyspnea, wheezing
CV: hypotension, shock
Skin: urticaria, angioedema, pruritus, erythema
GI: pain, nausea, diarrhea
Hematological: thrombocytopenia, DIC

25
Q

How does epinephrine counteract the disease state during anaphylaxis?

A

Vascular smooth muscle contraction, increased cardiac output, and inhibit mast cell degranulation

26
Q

Hygiene hypothesis

A
  • Allergy is on the rise in developed countries
  • Treg cells and IL-10 production capacity are low
  • skew towards Th2 response
    • IgE, IL-4, IL-5, IL-13
27
Q

Function of chemokines in type I hypersensitivity

A

Recruit PMNs, monocytes, and macrophages

28
Q

Late-phase reaction in immediate hypersensitivity

A
  • Few hours post exposure
  • Accumulation of PMNs, eosinophils, basophils, T helper cells, and their mediators
  • May occur without prominent immediate reaction
29
Q

Immediate hypersensitivity clinical responses

A
  • Food/drug allergies (hives, anaphylaxis, flushing, angioedema)
  • Atopic dermatitis (eczema)
  • Atopic urticaria (hives)
  • Atopic rhinoconjunctivitis (allergic rhinitis, hay fever)
  • Asthma
30
Q

Genetics of atopy (reaction to allergen)

A

MHCII, TCR-alpha, IL-4, FcεRI, and Th1/2 balance

31
Q

IL-10 function

A
  • Elevated in helminth infested individuals

- Blocks mast cell degranulation

32
Q

Type I hypersensitivity diagnostics

A
  • Application (skin prick or intradermal injection) of allergen in skin to visualize wheal and flare
  • Blood test to detect specific IgE (results take days)
33
Q

Type I desensitization

A

To gradually decrease IgE-dominant response towards IgG or Treg response (IL-10)

34
Q

Type II hypersensitivity

A
  • Antibody mediated disease caused by anti-tissue antibody
  • Main antibody – IgG, IgM
  • Antibody targets tissues or extracellular matrix
  • 2 - 24 hours
35
Q

Effector mechanisms of type II hypersensitivity

A
  1. ) Opsonization and phagocytosis
  2. ) Complement and Fc receptor-mediated inflammation
  3. ) Abnormal physiologic response w/o injury
36
Q

HDNB

A

Rh- mothers may carry an Rh+ fetus; fetal erythrocytes enter mother’s circulation during childbirth and anti-Rh antibodies produced in the mother; subsequent pregnancies in which the fetus is Rh+ may result in fetal erythrocyte destruction due to IgG crossing placenta (RhIG administration w/i 72 hours after first Rh+ birth)

37
Q

Type II hypersensitivity reactions

A 
Blood transfusions 
Autoimmune hemolytic anemias
Autoimmune thrombocytopenic purpura
Goodpasture syndrome
Pemphigus vulgaris
Penicillin sensitivity (non allergic) 
Acute rheumatic fever
38
Q

Grave’s

A

receptor of thyroid gland targeted by TSI (triggers production of TSH); symptoms: irregular heartbeat, bulging eyes, anxiety, heat sensitivity, weight loss, goiter

39
Q

Myasthenia gravis

A
  • Autoantibody targets acetylcholine receptors
  • Blocks acetylcholine binding, resulting in defective neuromuscular transmission
  • Symptoms: muscle weakness, localized paralysis, strabismus (eye misalignment), ptosis (drooping eyelids), difficulty swallowing
40
Q

Type III hypersensitivity

A
  • Antibody mediated disease caused by immune complexes
  • Main antibody – IgG, IgM
  • Antibody targets soluble antigen
  • Hours, days, weeks
41
Q

Effector mechanisms of type III hypersensitivity

A
  • Immune complex formation (normally cleared by classical complement and phagocytes)
  • Certain immune complexes may get deposited on tissue
  • Phagocytes (PMNs) recognize antibody via Fc receptors and complement via CRs (receptors activate cells to secrete inflammatory mediators»tissue inflammation and injury)
42
Q

Most common sites of immune complex deposition

A 
Small arteries (vasculitis)
Renal glomeruli (nephritis)
Joint synovium (arthritis)
43
Q

Serum sickness

A
  • Individuals w/ no prior exposure
  • Antitoxin administration from horse serum
  • Controls toxin but mounts response against horse antibodies
  • Symptoms: fever, weakness, rash, edema (7-21 days later)
44
Q

Arthus reaction

A
  • Localized form of type III hypersensitivity that causes vasculitis
  • Subcutaneous antigen is delivered to a previously immunized individual to that antigen
  • Antibody-antigen complexes form in the area of injection
  • Symptoms: inflammation, pain, and necrosis in severe cases
45
Q

Type III hypersensitivity reactions

A

Systemic lupus erythematosus
Polyarteritis nodosa
Granulomatosis with polyangiitis (Wegener’s disease)
Farmer’s lung

46
Q

Type IV hypersensitivity

A

-Type IV hypersensitivity is also delayed type hypersensitivity (DTH)
-Cell-mediated reaction
Th1
Th2
CTL (CD8+)
-2 days to weeks post exposure

47
Q

Effector mechanisms of type IV

A

-Antigen processed by APC,
-Th1 activated (IFN-gamma, macrophage activation and inflammatory mediators released)»tissue damage
-Th2 cells are activated
IL-5 – Eosinophil activation and inflammatory mediators released»tissue damage
-Th17 cell are activated
IL-17 – PMN recruitment and activation»tissue damage
-CTL activation – direct cytotoxicity of recognized MHCI-antigen

48
Q

Basis of tuberculin/PPD/Mantoux test

A
  • Individuals who have had Mycobacterium tuberculosis infection have produced memory CD4+ T cells to mycobacterial antigens
  • Exposure to PPD (tuberculin purified protein derivative) will activate these memory CD4+ T cells, release proinflammatory cytokines, and recruit macrophage, resulting in an indurated skin lesion 48-72 hours later
49
Q

Allergic contact dermatitis

A
  • skin inflammation including pruritic papules and vesicles on an erythematous base
  • Upon first contact with an allergen, sensitization may take 10 - 14 days (Langerhans cells (DCs))
    • Subsequent contact = hours to days (T cell mediated)
  • most common chemicals that cause ACD are:
    • Nickel Preservatives, dyes, and fragrances
    • Chemicals in rubber gloves
  • Many are haptens
50
Q

Poison Ivy

A
  • ACD reaction
  • component of plant penetrates skin and associated with proteins in keratinocytes
  • Primary exposure: memory T cells
  • Secondary exposure: Th1, macrophage, and CTL cells target skin
51
Q

Chronic DTH reactions

A
  • Cell types involved derived from macrophages
    • Epithelioid cells
    • Multinucleated giant cells
  • Tissue damage due to size and location of granuloma
  • Granulomas often form in diseases with persistent antigen
    • Tuberculosis
    • Leprosy
    • Leishmaniasis
52
Q

Type IV hypersensitivity reactions

A 
Hashimoto thyroiditis
Rheumatoid arthritis
Type I Diabetes
Celiac disease
Crohn disease
Multiple Sclerosis

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