Test 3: Immediate type hypersensitivity

Question 1

What are individuals called who have a response to allergens?

Answer 1

Atopic

Question 2

Does immediate type hypersensitivity occur after first or second exposure?

Answer 2

Second (unlike serum sickness)

Question 3

Put the sequence of events in order:
– Release of mast cell mediators
– Binding of IgE to Fcε receptors on mast cells or
basophils
– Production of IgE in response to an antigen
– Cross-linking of the bound IgE by “reintroduced”
antigen.

Answer 3

– Production of IgE in response to an antigen.
– Binding of IgE to Fcε receptors on mast cells or
basophils
– Cross-linking of the bound IgE by “reintroduced”
antigen.
– Release of mast cell mediators.

Question 4

What are some features of allergens?

Answer 4

• low molecular weight proteins
• glycosylated
• highly soluble
• many are enzymes

Question 5

How do most allergens enter the body?

Answer 5

skin/mucosa such as respiratory/GI tract

Question 6

Is there a genetic predisposition for allergies?

Answer 6

Yes–genetics influences ability to make IgE

Question 7

How much IgE is in serum and what is the half life?

Answer 7

1 microgram/mL; half life is 2-3 days (unless bound)

Question 8

What are the major cytokines released by TH2 cells and what are their functions?

Answer 8

IL-4: isotype switching to IgE and eosinophil recruitment
IL-5: eosinophil activation
IL-13: same as 4 with regulation of inflammation

Question 9

Where do mast cells come from and where do they mature?

Answer 9

Derived in bone marrow but travel to peripheral tissue and mature in situ

Question 10

What are the two types of mast cells?

Answer 10

• Mucosal mast cells: Very little histamine

- CT Mast cells: large amounts of histamine

Question 11

Where do basophils mature?

Answer 11

In bone marrow, <1% leukocytes

Question 12

What part of the Fc epsilon RI receptor has a high affinity for IgE?

Answer 12

Alpha chain

Question 13

What is sensitization?

Answer 13

Binding of IgE to the high affinity receptors on a mast cell in a non-specific manner

Question 14

What causes activation of mast cells?

Answer 14

Binding of 2nd exposure antigens–>cross linking of receptors

Question 15

What are the responses of the activated mast cells?

Answer 15

• Degranulation (primary mediator)
• Synthesis/secretion of lipid mediators (secondary)
• Synthesis/secretion of cytokines (secondary)

Question 16

What else can activate mast cells/basophils?

Answer 16

-anaphylatoxins (C5a) and some drugs

Question 17

When histamine is released and attaches to H1 receptors, what are the effects?

Answer 17

• endothelial cell constriction=capillary leakiness
• smooth muscle relaxants are produced=vasodilation/erythema
• bronchial smooth muscle constriction=bronchospasm and more mucous
• intestinal smooth muscle constriction=peristalsis

Question 18

Which receptor effects can be inhibited by antihistamines?

Answer 18

H1

Question 19

What are the effects of H2 receptors?

Answer 19

gastric acid and airway mucous secretion

Question 20

What drugs inhibit H2 receptors?

Answer 20

-cimetidine(tagamet), ranitidine(zantac), famotidine(pepcid)

Question 21

What are the 3 lipid mediators synthesized in mast cells (comes from arachidonate that is taken from cell membrane via phospholipase A2)

Answer 21

• Prostaglandin D2: COX pathway for vasodilation and bronchoconstriction
• Leukotriene C4: lipooxygenase pathway that does the same as histamine but lasts longer
• Platelet Activating Factor: bronchoconstriction and vascular permeability

Question 22

What are some of the cytokines released from mast cells? (late-phase rxn)

Answer 22

IL-3, TNF-alpha; TH2 cytokines

Question 23

What is the major cellular component in late phase reaction?

Answer 23

Eosinophils; effects from immediate response can return hours later, kills parasites and can damage tissue

Question 24

What are the 3 phases from immediate hypersensitivity manifestations upon intradermal administration? (associated with histamine)

Answer 24

1: erythema
2: central area becomes edamatous and blanches (plasma leakage from post-cap venules)=WHEAL
3: marginal perimeter erythematous=FLARE

Question 25

What is caused by increased permeability of vessels in the skin and subcutaneous tissues?

Answer 25

Urticaria (hives) and angioedema

Question 26

What is the most common manifestation of immediate hypersensitivity?

Answer 26

Hay fever/allergic Rhinitis

Question 27

What are some symptoms of hay fever?

Answer 27

• watery rhinorrhea, sneezing, pruritis of nose and palate, eye itching and redness and tearing
• associated with histamine release along with Leukotrines and PGD

Question 28

What type of asthma is caused by immediate type hypersensitivity?

Answer 28

Extrinsic asthma

Question 29

What mediates the asthma?

Answer 29

Leukotrines and prostaglandins (from mucosal mast cells–not a lot of histamine)

Question 30

What are the cardio effects of anaphylactic shock?

Answer 30

• general arterial vasodilation and increased vascular permeability–>hypotension and shock
• cardiac ischemia from hypotension

Question 31

What are the respiratory and GI effects of anaphylactic shock?

Answer 31

smooth muscle constriction–mucous plugging airways; cramping, nausea, vomiting

Question 32

What is involved in desensitization?

Answer 32

• sterile aggregated antigens injected subcutaneously in increasing doses until a small local area of inflammation is reached
• this is a maintenance dose that is used for years
• shifts Ig production to IgG instead of IgE=blocking antibody