Allergy/Immunology 1 Flashcards
1
Q
Plasma cells (3)
A
- Secrete antibodies, antiglobulins
- New guidelines say need to check IgE levels before giving peanuts at 6 months
- Introduce only if you do a skin prick test; way of introducing peanuts earlier
2
Q
IgA (5)
A
- IgA is lining your respiratory tract; takes 6 weeks for tract to regenerate
- Kids that are IgA deficient – the most common form of immune deficiency
- Think about with recurrent respiratory diseases, sinusitis, otitis
- Provides antibodies in mucous and saliva
- Activates alternate compliment pathway
3
Q
IgE (2)
A
- plays a role in allergy, mast cell degranulation, immediate release of histamine
- Main player = degranulation of mast cell
4
Q
IgG (2)
A
- Long term antibodies
2. Measles outbreak = once you get the disease have long-term protection*
5
Q
IgM
A
acute antibody; take an example of EBV you do not order an IgM at the very beginning and you want to wait 6-7 days
6
Q
Allergic Reactions (3)
A
- Allergy – Results as part of a specific acquired alteration in the body that has an immunologic basis.
- Union of antigen and antibody – Cascade of events that culminates in biochemical reactions.
- All four types of allergic reactions – Mediated by circulating or cellular antibodies
7
Q
TH1 Cells (3)
A
- Infectious
- Seeing more allergies = vaccinations have caused less infections and a shift towards TH2 end
- Kids who live in farms get exposed early and shift towards TH1 end
8
Q
Mast cell chemical activation: histamine (2)
A
- Bronchoconstriction, mucus production, vasodilatation, pruritus, arrhythmias, chemoattractant
- Rales in asthma because of mucous production
9
Q
Mast cell chemical activation: Prostaglandins D-2 (PGD2)
A
Bronchoconstrictor, peripheral vasodilator, coronary vasoconstrictor, neutrophil chemoattractant
10
Q
Mast cell chemical activation: platelet activating factor
A
Bronchoconstrictor, vasodilator, chemotaxis, degranulation of neutrophils
11
Q
Mast cell chemical activation: leukotriene B4
A
Neutrophil chemotaxis
-Too many neutrophils cause a lot of destruction
12
Q
Mast cell chemical activation: Leukotriene C4 and Leukotriene D 4(LTC4 & LTD4)
A
Bronchoconstrictor, increase vascular permeability, chemotaxis
13
Q
Type 1 Allergic Reaction (6)
A
- IgE mediated!
- Local and systemic manifestations resulting interaction between antigen and tissue cells
- Allergen interacts with IgE antibody on the surface of mast cells and basophils resulting in the cross link of IgE, Fc€RI receptor apposition and mediator release from these cells
- Histamine and release of IgE = type 1 allergic reaction and can cause urticaria
- Anaphylaxis = type 1 reaction
- Systemic and local reactions, cardiac involvement, GI involvement
- Involves IgE and histamine
14
Q
Step 1 of IgE mediated sensitivity (4)
A
Type 1 allergic reaction
- Sensitization
- Initial exposure leading to increase in allergen specific IgE
- Cell mediator symptoms increase
- Occurs within minutes of subsequent exposure to antigen with release of mediators such as histamine
15
Q
Step 2 of IgE mediated sensitivity (2)
A
- Early Phase minutes
2. Mast cells release histamine and leukotrienes and cytokines
16
Q
Step 3 of IgE mediated sensitivity (3)
A
- Late phase: hours
- Late phase = one of the reasons if mom doesn’t fill prescription is even worse
- Inflammation of respiratory tract
17
Q
What produces IgE?
A
plasma cells
18
Q
Clinical criteria for diagnosis of anaphylaxis (3)
A
- Acute onset of an illness (minutes to several hours) with involvement of skin, mucosal tissues, or both (e.g. generalized hives, pruritus, or flushing) and at least one of the following: respiratory compromise or reduced BP or associated symptoms of end-organ dysfunction
- Two or more of the following that occur rapidly after exposure to a likely allergen for that patient – involvement of the skin-mucosal tissue, respiratory compromise, reduced BP, or persistent GI symptoms
- Reduced BP after exposure to a known allergen or greater than 30% decrease in systolic BP
19
Q
Factors that intensify anaphylaxis or interfere with treatment (5)
A
- Presence of asthma
- Underlying cardiac disease, especially with rapid infusion of allergen, older individual
- Concominant therapy with B-adrenergic, b1/b2 antagonists, monaomine oxidase inhibitors, tricyclics, ACE inhibitors, ARBs
- delay or inadequate dose of Epi
- psychiatric disease
20
Q
Clinical manifestations of type 1 reaction: two phases (6)
A
- Immediate allergic reactions
a. Sneezing
b. Hives
c. Wheezing
d. Vomiting
e. Anaphylaxis - Late-phase response
a. Release of toxic mediators by activated eosinophils and mononuclear cells recruited to the site of the acute allergic reaction
21
Q
what causes the late phase reaction? (9)
A
- Mast cells
- T cells
- Mediators at post capillary endothelial cells
- Adhesion of circulating leukocytes
- Infiltration of tissues by eosinophils, neutrophils and basophils
* Eosinophils produce mediators that promote tissue damage - Outflow of plasma leading to local edema.
- TH2 lymphocytes release cytokines (interleukon and interferon) that promote IgE production
- Eosinophil chemoattraction
- Increased numbers of mucosal mast cells
22
Q
Urticaria
A
PART OF TYPE 1 REACTIONS; hallmark is they move
23
Q
Clues of allergic rhinitis (4)
A
- nasal itching
- mouth breathing
- allergic shiners
- repeated nose rubbing “allergic salute”
24
Q
Type II Allergic Reaction (2)
A
CYTOTOXIC REACTION
- IgG or IgM antibody is directed again antigens on the individual own tissue
- The binding of the antibody to the cell surface results in complement activation, signaling white blood cell influx and tissue injury
25
Examples of type II reactions (4)
1. Lung and kidney damage in Goodpasture syndrome
2. Acute graft rejection
3. Hemolytic disease of the newborn
4. Certain bullous skin dise1ases
26
Type III Allergic Reaction (3)
IMMUNE COMPLEX DISEASES
1. IgG and IgM antigen-antibody complexes of a critical size are not cleared from circulation
2. They fix in the small capillaries throughout the body
3. Leads to influx of inflammatory white blood cells resulting in tissue damage
27
Examples of Type III Reactions (3)
1. Serum sickness
- See kids coming in with swollen hands, faces, mild anemia
2. Lupus erythematosus
- Immune complex disease
3. Glomerulonephritis after common infection
28
Serum Sickness (8)
1. Fever
2. Lymphadenopathy
3. Joint Swelling
4. Rash – many different types
5. Culprits – Ceclor, penicillin
6. Serum Sickness
7. Swelling and did is on an antibiotic; HALLMARK IS SICK*
8. Erythema migrans
29
Type IV allergic reaction (4)
DELAYED-TYPE HYPERSENSITIVITY
1. T-cell antigen receptor of the Th1 lymphocytes bind to the tissue antigen
2. Result in clonal expansion of lymphocyte population
3. T-cell activation with release of inflammatory lymphokines
4. Involving sensitized lymphocytic cells that results in the release of toxic lymphoid cell-products
30
Examples of Type IV allergic reactions (3)
1. Tuberculin skin test reactions
* PPD = classic type IV reaction
2. Contact dermatitis
3. Leprosy or Hansen’s disease
31
Type IV-A1 Allergic reactions
Mediated by CD4 TH1 cells causing classic delayed *Allergic contact
32
Type IV-A2 Allergic reactions
Medicated by TH2 cells resulting in cell mediated hypersensitivity
*Asthma
33
Type IV-B1 Allergic reactions
Cytotoxic CD*+ cells that mediate graft rejection and Stevens Johnson syndrome
*Steven Johnson’s syndrome = lamictal
34
Type IV-B2 Allergic reactions
Mediated by CD8+ lymphocytes that produce IL-5, resulting in cell mediated eosinophilic hypersensitivity associated with viral mucosal infection
*Viral mucosal infection
35
Nonimmune Anaphylactic Reactions (Formerly Anaphylactoid Reactions) (5)
1. Drugs
a. Aspirin, NSAID, gammaglobulin, morphine, codeine, anesthesia medications
2. Physical causes
a. Exercise, cold, heat, sunlight
3. Exercise dependent food induced
4. Radio-contrast material
5. Idiopathic
36
Difference between allergy ad Atopic Disease (3)
1. Atopy is not interchangeable with allergy
2. Atopy is the inherited risk to develop IgE mediated responses following exposure to allergens and puts a person at greater risk for development of the atopic triad
3. Allergy involves hypersensitivity that occurs upon re-exposure to sensitizing allergens
37
Development of atopic disorder (2)
1. The development of an atopic disorder or allergic response involves
2. Susceptible individual who is both exposed to an offending antigen and has a predisposition to selective synthesis of immunoglobulin E (IgE) when in contact with common environmental antigens.
a. Try to avoid kids developing allergies even when they do have a tendency
b. Need to be exposed to antigen and have allergic tendency to avoid
38
Atopy (4)
1. Atopy is typically associated with a genetically determined capacity to mount IgE responses to common allergens especially inhaled allergens and food allergies
2. ALLERGIC RHINITIS
3. ASTHMA
4. ATOPIC DERMATITIS
39
Cascade of events with allergic reactions (6)
1. Contact with an offending antigen occurs
2. Brisk proliferation of T helper type 2 (Th2) cells
3. Secretions of cytokines: interleukin (IL)-3, IL-4, IL-5, IL-9, and IL-13; Cytokines are involved in IgE synthesis and activation of eosinophils.
4. TH2 cells are T cells that hit allergic side of reaction and bring on cytokines (interleukons and interferons) and cause a lot of inflammation
5. IgE binds to receptors on mast cells, basophils, and Langerhans cells.
6. Chemical mediators that cause biochemical reactions and allergic- related injury to target organs (skin and respiratory tract) are released.
a. Histamine
b. Prostaglandins
c. Leukotrienes
d. Eosinophil chemotactic factor of anaphylaxis
e. High-molecular-weight neutrophil chemotactic factor
f. Platelet-activating factor
g. Arachidonic acid—cyclo-oxygenase and lipoxygenase products
40
End result of allergic reaction (1-3d)
1. Tissue injury of a target organ
2. Inflammation and hyper-responsiveness
3. Symptoms
a. Airway obstruction
b. Increased mucus discharge
c. Pruritus
d. Some kids itch from urticarial, and some kids don’t; depends on individual
