Asthma Flashcards

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1
Q

The pathogenetic process underlying allergic airway disease is initiated by __________ lymphocyte proliferation. How are these lymphocytes proliferated?

A

TH2

  1. An antigen is taken up by an antigen presenting cell
  2. The antigen is then presented to Th0, which can differentiate into either Th1 or Th2.
  3. Th0 is differentiated in Th1 in the presence of IL-12 and IL-18, IFN-gamma prevents the differentiation into Th2.
  4. The presence of IL-4 allows the differentiation into Th2.
  5. Th2 then release IL-3, IL-4, IL-5, IL-9, IL-10, IL-13
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2
Q

What happens once proliferation of Th2 is stimulated?

A
  1. Th2 releases IL-4 and IL-13, which stimulates production IgE from B lymphocytes.
  2. IL-3, IL-4, IL-6, IL-9, and Stem cell factor make IgE bind to basophils or mast cells.
  3. Th2 also releases IL-3, IL-5, and GM-CSF to stimulate eosinophil production and activity.
  4. Eosinophils, Basophils, and Mast cells release an array of mediators, cytokines, and chemokines.
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3
Q

What are the two signals required for class switching?

A
  1. The first signal is delivered from IL-4 or IL-13, which induce B cells to initiate transcription of germ-line emRNA for IgE antibodies.
  2. Signal 2 is the binding of Cd40 to the CD40 ligand, which causes gene rearrangement.
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4
Q

. Specific high-affinity receptors (___________) on mast cells, basophils, and Langerhans’ cells bind through the constant (Fc) region of IgE antibodies.

A

FcεRI

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5
Q

_________________- is the key event that launches the symptoms of the early allergic response.

A

Mast cell degranulation

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6
Q

What components do mast cells release? What effect does this have?

A

Mast cells release preformed mediators (especially histamine and proteases) and newly produced lipid mediators, including PGD2 and LTC4, that promote inflammation and are thought to be responsible for the smooth muscle contraction and airway mucosal edema that are seen in the acute response.

Mast cells can also produce many cytokines, such as IL-4 and IL-13, that can enhance IgE synthesis and contribute to the persistence of allergic inflammation and tissue remodeling.

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7
Q

The ____________ and the ____________are the major effector cells in allergic inflammation.

A

mast cell; eosinophil

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8
Q

-Interactions between the adhesion molecules (____________ and ____________) is important
for the cells to be able to enter the tissues.

A

VCAM; ICAM

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9
Q

What is asthma?

A

○ A chronic inflammatory disorder of the airways.
▪ Wheezing
▪ Chest tightness
▪ Dyspnea-shortness of breath
▪ Airway obstruction is reversible
There’s also increased bronchial hyper-responsiveness; meaning
their airways’ are twitchy, kind of like when someone blows
really hard and then starts coughing.

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10
Q

Type of hypersensitivity implicated in Asthma?

A

Type I (IgE)

Type IV (Delayed)

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11
Q

Different components are released from mast cells/ basophils at different times. What components are released at immediately, over minutes, and over hours?

A

Immediate release

  • Granule contents (Histamine, TNFa, Proteases, Heparin)

Over Minutes

  • Lipid Mediators (Prostaglandins, Leukotrienes)

Over Hours

  • Cytokine production (IL-4 and IL-13)
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12
Q

Cells involved in asthma

A

Broncial epithelium

Th cells

Mast cells

Eosinophils

Neutrophils

Airway Smooth muscle

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13
Q

Airway remodeling is due to _________

A

Mucosal inflammation

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14
Q
A
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15
Q

Immunotherapy increase __________cells

A

IL10+ T

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16
Q

Strategies against ____________ameliorate asthma.

A

T lymphocytes

17
Q

What is the role of immunotherapy?

A

Tolerance. Makes the body tolerant to the antigen.

Reduces IgE affinity

18
Q

What does IL-10 do?

A

Blocks costimulation (B7 and CD28) and subsequent T cell signaling

Suppresses T cells along with TGFBeta

19
Q

Effects of Leukotriene C

A

Bronchoconstriction

Vascular permeability

Mucous secretion

Chemotaxis

20
Q

Effects of Histamine

A

Bronchoconstriction

Vascular permeability

21
Q

Effects of Prostaglandin

A

Bronchoconstriction

Vascular permeability

Mucus Secretion

22
Q

Effects of TNFa

A

Tissue injury

Cell recruitment

23
Q
A
24
Q

Effects of Proteases

A

Tissue Injury

Mucous Production

25
Q

Mast Cell Tryptase in Asthma

A

Bronchoconstriction

Bronchial hyper-responsiveness

Stimulation of proliferation of fibroblast, smooth muscle, and epithelial cells

Generation of kinins

Stimulation of IL-8 release

Eosinophil chemotaxis

26
Q

Monoclonal Antibodies

A

Mepolizumab

Reslizumab

Benralizumab

Tezepelumab

27
Q

Gene related to asthma susceptibility related to the epithelial mesenchymal tropic unity

A

ADAM33

28
Q

Possible side effects to Inhaled Corticosteriods

A

Bruising

Decreased bone density

Suppression of HPA-axis

Growth suppression

Dysphonia, thrush

29
Q

Not appropriate for monotherapy

A

Beta2-agonists

30
Q

If penicillin is given and within minutes the patients throat closes off, what type of reaction is that?

A

Type I

31
Q

12 year old not controlled with allbutoron alone, what drug do add?

A

Inhaled corticosteriods

32
Q

What medications would you use to mimic the effects of asthma that you could use diagnostically?

A

Methacholine

33
Q

When does the delayed response occur?

A

6-8 hours or more

34
Q

What cells are most important in causes anaphylaxis?

A

Mast cells

35
Q

If you’re stung by a bee and you anaphylas, what cell type does the venom bind to?

A

Mast Cell

36
Q

Anaphylactoid reactions

A

produce the same clinical picture with anaphylaxis but are not IgE mediated, occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation.

37
Q
A