Hypersensitivity Disorders

Question 1

Type I

Answer 1

Mediated by IgE and results from mediators secreted by mast cells

Question 2

Type II

Answer 2

Mediated by Abs that bind tissue Ags and cause complement-dependent tissue injury and disease

Question 3

Type III

Answer 3

Mediated by circulating Ab-Ag complexes which deposit in vessels and cause complement-dependent injury in the vessel wall (vasculitis)

Question 4

Type IV

Answer 4

Mediated by T cells and results from inflammation caused by cytokines released by Th1 and Th17 cells, macrophages, or killing of host cells by CD8 CTLs
-Also known as DTH delayed type hypersensitivity

Question 5

Histamine function

Answer 5

Dilation of small vessels and vascular permeability

Question 6

Protease, prostaglandins, leukotrienes, cytokines all do what

Answer 6

Proteases- cause local tissue damage
Prostaglandins- Vascular dilation
Leukotrienes- Smooth muscle contraction
Cytokines- local inflammation

Question 7

Sequence of events in immediate hypersensitivity reactions (type I)

Answer 7

Primary exposure to allergen activates Th2 cells and IgE is produced
Binding of IgE to Fce receptors- patient is sensitized
Secondary exposure- Ag dependent cross-linking of membrane bound IgE causes activation of mast cells and release of inflammatory mediators

Question 8

Immediate vs late phase reaction in Type I

Answer 8

Immediate vascular/smooth muscle reactions characterized by vasodilation, congestion, edema
Late phase- 2-24hrs later- inflammatory infiltrate rich in eosinophils, neutrophils and T cells

Question 9

Anaphylaxis

Answer 9

Food allergen exposure causes massive release of vasoactive amines/cytokines from mast cells throughout body
Drop in blood pressure resulting in vascular shock
Contraction of smooth muscle in bronchi making breathing difficult

Question 10

Key mechanism of allergen specific immunotherapy

Answer 10

Generation of induced regulatory Treg cells

Question 11

Type II hypersensitivity method of action

Answer 11

IgG/IgM Abs activated complement system resulting in C3a/C5a production
Neutrophil/macrophages activated in FcR/CR1 dependent manner release ROS/lysosomal enzymes causing damage

Question 12

Graves disease/myasthenia gravis cause

Answer 12

Abs bind and stimulate activity of TSH receptors even in absence of TSH- Graves
Abs inhibit binding of Ach to Ach receptor causing myasthenia gravis

Question 13

Penicillin induced anemia

Answer 13

Drug binds directly to erythrocyte surface and induces anti-drug Ab
Improves after stopping Abx

Question 14

Quanidine induced anemia

Answer 14

Autoantibodies form immune complexes with drug
Complexes bind erythrocyte surface through CR1
May require immunosuppression/plasmapheresis to remove complexes

Question 15

Methyldopa induced anemia

Answer 15

Drug induces antidrug Ab that cross reacts with an Rh antigen