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Allergy and hypersensitivity Flashcards

1
Q

Inflammation 1

A
  • Physiologic response to injury (physical, chemical, biologic)
  • Characterized by cellular and biochemical changes leading to clinical manifestations
  • Cellular changes: vasodilation/leakage, leukocyte infiltration, local hypoxia, secondary tissue damage
  • Biochemical changes: inflammatory mediator release (histamine, cytokines, eicosanoids)
  • Complement, kinin, coag systems activated
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2
Q

Inflammaiton 2

A
  • Clinical manifestations: redness, hot, swelling, pain, loss of function (LOF)
  • Immune system initiates, amplifies, and regulates Ag-specific or molecular pattern-specific inflammatory responses
  • Good inflammation: repair, healing, recovery
  • Bad inflammation: persistent cellular and biochemical changes, chronic clinical manifestations, LOF, cancer, atherosclerosis
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3
Q

Hypersensitivity

A
  • Heightened host responsiveness to normally innocuous substances (4 types)
  • Type I: mast cell/IgE induced
  • Type II/III: IgM/IgG and complement induced
  • Type IV: CD4/CD8 mediated
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4
Q

Allergy

A

-Immunologically mediated hypersensitivity; IgE mediated vs other mechanisms

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5
Q

Atopy

A

-Genetic predisposition to IgE-mediated response

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6
Q

Role of the Th2 CD4 cell

A
  • Th2 cells induce B cells to switch to IgE Abs (responsible for allergy, asthma)
  • Th1 and Th17 responsible for autoimmune diseases (along w/ lack of Tregs)
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7
Q

IgE-mediated hypersensitivity

A
  • Th2 cell presenting innocuous Ag on MHC binds to B cell, along w/ co-stimulator
  • Th2 cell remodels cytoskeleton and begins releasing IL4
  • IL4 is released btwn into the cellular synapse and activates the B cell, causing a switch to IgE producing plasma cell
  • Both cells also undergo membrane changes
  • IgE/Ag complexes bind to Fc(epsilon) receptor on mast cell and causes granule release (histamine, ect)
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8
Q

Type I hypersensitivity

A
  • Immediate hypersensitivity; Th2, IgE, mast cells, eosinophils involved
  • Mast cell-derived mediators released due to IgE-Ag complex binding to Fc receptor of the mast cell
  • Also have cytokine-mediated inflammation due to eosinophils/PMNs
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9
Q

Type II hypersensitivity

A
  • Ab-mediated diseases; IgM, IgG Abs against cell surface or ECM Ags
  • Complement and Fc receptor mediated recruitment and activation of PMNs and macrophages (complement not required)
  • Opsonization and phagocytosis of cells
  • Abnormalities in cellular function function can lead to tissue damage
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10
Q

Type III hypersensitivity

A
  • Immune complex-mediated disease; Immune complexes of circulating Ags-IgM/G are deposited in vascular basement membrane (inflammation of vessel wall = vasculitis)
  • Complement and Fc receptor-mediated recruitment and activation of WBCs
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11
Q

Type IV hypersensitivity

A
  • CD4 (Th1) T cells produce delayed type hypersensitivity rxn (activating macrophages), not Abs required
  • Extended time from Ag exposure to observed response
  • CD8 CTLs produce cytolysis
  • Macrophage activation and cytokine mediated inflammation (no histamine released)
  • Contact dermatitis is type IV, so is type I diabetes
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12
Q

IgE and its production

A
  • Mast cells and basophils express high affinity receptor Fc(e)
  • MHC specificity determines who gets allergic to what
  • Environment plays a role; exposure to allergens/microbes drives the change from Th2->Th1 CD4 cells
  • This reduces allergic rxns (hygiene hypothesis)
  • Microbiome of gut also shapes allergen susceptibility
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13
Q

Pathways in generating allergy and asthma 1

A
  • Impaired epithelial barrier (infection, allergen exposure) mostly in U and L RT, GI, and skin
  • Generation of thymic stromal lymphopoietin (TSLP) by local epithelial cells, fibroblasts, and mast cells
  • TSLP activates immature dendritic cells to drive Th2 production, leading to more IL4 and 13 (IgE switch) and IL5 (eosinophil activation)
  • Damaged epithelium can also drive inflammation
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14
Q

Pathways in generating allergy and asthma 2

A
  • Overall there is a net reduction in IL12 (decreases Th1), a net increase in IgE (IL4 and 13) and an increase in eosinophils (IL5)
  • IgE mediates inflammatory cascade involving mast cells, basophils, eosinophils, and inflammatory mediators
  • IL13 induces SMC proliferation, mucus hypersecretion, goblet cell metaplasia, eosinophil recruitment, fibrosis (asthma)
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15
Q

Mast cell vs Basophil

A
  • Mast cells are mononuclear and found in tissue
  • Basophils are polynuclear and found in blood
  • They both have metachromatic granules, release inflammatory mediators, and have Fc(e) receptor
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16
Q

Activation of mast cells

A
  • Fc(e) receptors must be dimerized (both bound to IgE/Ag complex) to activate signaling pathway
  • Granule contents: histamine (acute phase rxn 10-20 min), prostaglandins, leukotrienes, cytokines (late phase rxn 4-8 hrs)
  • Acute phase: edema
  • Late phase: cellular infiltrate
17
Q

Eosinophils

A
  • Protein-containing granules (major basic protein, cationic protein, neurotoxin)
  • Th2 and IL5 directed production and activation
  • Release cytokines IL1, TNFa, TGBa/b
  • Effector functions: ADCC (Ab-dependent cell cytotoxicity) for destruction of helminths, also host tissue damage
18
Q

Dx of IgE mediated allergy

A
  • IgE serum level
  • RAST (radioallergosorbent test): in vitro Ag-sepecific IgE test
  • Skin test (done to confirm Dx)
19
Q

Rx of IgE-mediated disorders

A
  • Allergen avoidance
  • Symptomatic Rx (antihistamines, leukotriene inhibitors, bronchodilators)
  • Immunomodulation(corticosteroids, specific immunotherapy, anti-IgE monoclonal Ab)
  • Specific immunotherapy (allergy shots)
  • Advantages of aerosol vs oral: lower dosage, rapid onset, fewer side effects, direct delivery to airways
20
Q

Wheeze vs stridor

A
  • Wheeze is high pitch whistling sound on expiration

- Stridor is the same thing but on inspiration

21
Q

Allergic rhinitis and conjunctivitis

A
  • Itchy, watery eyes w/ stuffy nose
  • Itchiness is most common factor in allergic rxns
  • Most common triggers: dust mites, pollen, mold, irritants (smoke)
22
Q

Things that increase one’s risk to allergies

A
  • Race
  • Family Hx
  • Lack of brest feeding
  • Lack of exposure to Ags early on
  • Destruction of gut microbiome

Blood (30 decks)

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