Hypersensitivities

Question 1

Type I: Immediate-type hypersensitivity reactions

Answer 1

initiated by mast cell degranulation mediated by cross-linking of IgE to IgE fc receptors on mast cells
reactions occur within minutes

Question 2

Type II: altered self hypersensitivity reaction

Answer 2

initiated by allergen-specific IgG antibodies and inflammation is mediated by the complement cascade, phagocytes, and NK cells
takes 4-12 hours usually

Question 3

Type III: Immune complex hypersensitivity reaction

Answer 3

result from immune complex deposition into host tissues and the inflammatory responses that ensue when phagocytes try to clear the complex
end result is inflammation that is driven by complement activation and phagocyte-derived cytokines and chemokines
type II can sometimes develop into Type III
(IgG is the immune reactant in this case as well)

Question 4

Type IV: Delayed type hypersensitivity reaction

Answer 4

hypersensitivity response mediated by T cells (CD4 CD8 or both)
takes 24-72 hours

Question 5

T/F There must be a first exposure to the allergen in which the primary immune response is generated, but no symptoms of hypersensitivity are experienced. After that, any subsequent exposure to that allergen elicits the hypersensitivity response and any symptoms that go along with that response.

Answer 5

true

Question 6

Allergens that elicit IgE response and thus immediate-type hypersensitivity reaction

Answer 6

• must be proteins (must be proper T dependent cell antigens)
• often proteases
• low dose (driver differentiation from Th0 to Th2 needed for class switching to IgE)
• low molecular weight (can better diffuse out of dust particle)
• high solubility (will elute more efficiently from dust particle)
• highly stable (must survive as desiccated particle)
• contain peptide that binds to MHC class II

Question 7

Mast cell granules

Answer 7

• tryptase, chymase, cathepsin G, carboxypeptidase-remodel connective tissue matrix
• histamine***, heparin-increase vascular permeability,cause smooth muscle contraction, toxic to parasites
• TNF-alpha (some stored preformed in granules)-promotes inflammation, stimulate cytokine production, activates endothelium
• IL-4, IL-13-stimulate and amplify Th2 response
• Leukotrienes C4, D4, E4-smooth muscle contraction, increase vascular permeability, mucus production

Question 8

wheel and flare reactions

Answer 8

hives

Question 9

primary role of mast cells

Answer 9

expulsion of parasites from the body

Question 10

mast cell degranulation in the GI tract

Answer 10

increased fluid secretion and peristalsis leading to vomiting and diarrhea to clear the upper and lower GI tract

Question 11

mast cell degranulation in the airway

Answer 11

increased mucus secretion and decreased diameter of the airways leading to coughing and sneezing to clear the airway

Question 12

mast cell degranulation in the blood

Answer 12

vascular endothelium activated causing fluid and proteins to move from the vasculature into the inflamed tissue pushing fluid containing antigens and APCs from the lymph to the secondary lymphoid tissues where T and B cells can become activated

Question 13

systemic degranulation of mast cells (anaphylactic shock)

Answer 13

• life threatening
• occurs if allergen gets into blood and is disseminated throughout the body
• causes rapid loss of blood volume leading to systemic edema and hypotension
• in the airway it causes contraction of smooth muscles and a compromised airway
• contraction in the GI tract leads to vomiting and diarrhea and further loss of fluids
• culminated in ANAPHYLACTIC SHOCK

Question 14

treatment for anaphylactic shock

Answer 14

epinephrine/adrenaline

reverses the effects of mast cell degranulation on vascular epithelium

Question 15

fecal matter of dust mites is an abundant source of______

Answer 15

proteolytic enzymes leading to mast cell response

Question 16

most noteable type II hypersensitivity reactions

Answer 16

abnormal response to penicillin-modified erythrocytes following treatment with penicillin

Question 17

type II hypersensitivity: penicillin-induced

Answer 17

• some penicillin binds to RBC’s and modified surface determinants
• complement cascade already initiated bc of ongoing infection so some C3B will be deposited on RBCs and macrophages will phagocytose
• macrophages can then present the altered determinants of RBCs to T cells
• T cells then activate B cells resulting in an antibody response against the altered RBC determinants
• antibodies bind to RBCs opsonizing them, and if the antibody isotype is one that fixes complement, RBCs will become coated with abundant C3b and will either be destroyed by MAC or taken up by phagocytes.

Question 18

T/F destruction of RBCs following penicillin treatment will occur until the altered determinants have been recycled off the surface of the RBCs

Answer 18

true

Question 19

Arthus Reaction

subcutaneous

Answer 19

• occurs when an allergen is introduced into tissues underlying the epithelium
• antibodies specific for the allergen activate the classical complement cascade
• resultant anaphylatoxins mediate inflammation directly and also binds to the C5a receptors on the mast cells underlying the epithelium
• results in mast cell degranulation (macrophages and neutrophils can also contribute to inflammatory response)

Question 20

systemic immune response disease

intravenous

Answer 20

• allergen gains access to the vasculature and a large (too large to be cleared) number of immune complexes ensue
• these become deposited along the vasculature and especially in the glomeruli of the kidneys
• inflammatory mediators result from the production of anaphylatoxins and phagocyte mediators
• results in vacillates, kidney dysfunction, and neurologic symptoms resulting from vasculitis in the brain
• PRESENTATION SIMILAR TO SEPTIC SHOCK

Question 21

farmer’s lung

inhaled

Answer 21

Immune complex hypersensitivities that result from inhalation of allergen

• inhaling mold spores and other allergens from hay
• occurs because pt works with the allergen daily

Question 22

Pigeon breeder’s disease, poultry workers lung, bird breeders disease

Answer 22

all names for a condition that results from inhaling allergens that are found in the droppings of birds

Question 23

delayed type hypersensitivity reactions

Answer 23

• most often mediated by Th1 cells and stimulates their effector responses
• chemokine production
• macrophage activation via IFN-gamma
• TNF-alpha and LT production to mediate local tissue destruction and increased expression of adhesion molecules
• IL-3 and GM-CSF production to increase monocyte production

Question 24

tuberculin reaction

Answer 24

• positive response to the tuberculin test is mediate by Th1 T cells and not seen until 2-3 days after the initial injection
• if pt received BCG vaccine the test will be positive

Question 25

poison ivy (naturally occurring DHT response)

Answer 25

• caused by pentadecacatechol oil
• penetrates the skin and causes alteration of the normal self determinants underlying the tissue
• response by Th1 and CTLs
• contact hypersensitivity, similar results with nickel
• **remember you won’t get rash the first time you’re exposed

Question 26

T/F some people that can be exposed to poison ivy plants without ever making the allergic response. This is likely related to their MHC haplotype; if they cannot present the altered determinant because their MHC class I or MHC class II isoforms will not bind to those peptides, that person will not be able to make the immune response

Answer 26

true