Mechanisms of Immune Injury (Hypersensitivity Reactions) Handout Flashcards Preview

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Flashcards in Mechanisms of Immune Injury (Hypersensitivity Reactions) Handout Deck (21)
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1
Q

Type 1 Initiation

A

Production of IgE antibodies because CD4 cells of Th2 type favored over Th1….Th2 cells secrete IL-4 and turn on IgE producing B cells…IgE attaches to mast cells and basophils using Fc receptors to arm them

2
Q

Type 1 exposure second time

A

Binding and bridging of IgE antibodies causes release of primary and secondary meidators

3
Q

Type 1 primary mediators

A

Histamine (quick and short lived)

4
Q

Type 1 secondayr mediators

A

Leukotrienes (begins later and longer liver)

5
Q

What do type 1 mediators result in?

A

Cellular infiltration, vasodilation, increased permeability, and smooth muscle spasm

6
Q

Local reactions of Type 1

A

Allergic rhinitis
Uticaria
Angioedema
Asthma

7
Q

Systemic reaction of Type 1

A

Anaphylaxis…happens when gained access to vasculature…generalized itching to respiratory distress…can cause death

8
Q

Type 2 complement dependent

A

IgG or IgM attaches to cell surface and complement activated…MAC pokes holes…C3a and C5a recruit inflam cells…C3b opsonizes

Transfusion rxns, erythroblastosis fetalis, AI hemolytic anemai, Good pasture syndrome

9
Q

ADCC

A

Complement independent…effector cells posses Fc receptors that attach to target cells coated with IgG.

Tumor cell destruction and parasite destruction

10
Q

AB mediated cellular dysfunction

A

AB involved but no inflammation or destruction.
MG - antibodies block Ach receptors
Graves- AB stimulate TSHR

11
Q

Type 3 hypersensitivity

A

Immune complex related

SLE, glomerulonephritis, Serum sickness

12
Q

Immune complex tissue pathology determinants

A

Size - smaller are more phagocytic because they can survive
Mononuclear phagocytic system - dysfunction of these can reduce elimination
Valency/avidity of AB, affinity of antigen to tissue componendts, 3D strucutre of complex, hemodynamic factors

13
Q

Favored areas of immune complex formation

A

Filter barriers like glomerular basement membrane in kidney or synovial membranes in joints

14
Q

Tissue injury type 3 phase 1

A

Formation of Complex…about a week

15
Q

Tissue injury type 3 phase 2

A

Deposition of complex in tissues…facilitated by vascular permeability that comes about from cytokines being released after complex interacts with inflam cells

16
Q

Tiasue injury type 3 phase 3

A

Complement activation and inflam cell activation results in inflam reaction…coagulation cascade activation and platelet aggregation…about 10 days

17
Q

Local immune complex dz

A

Arthus rxn
Localized area of tissue necrosis from acute immune complex vasculitis
Typical reaction peaks 4-10 hours after injection…complexes formed at site of injection

18
Q

Type 4 rxns

A

DTH and T cell mediated cytotoxicity

19
Q

DTH

A

Must have been sensitized…reexposrue activates Th1 cells to secrete IL-12, TNFalpha, IL-2, IFNgamma…activated macrohpages attempt to remove agent…if they can’t granulomatous inflammation occurs

Examples in TB test, contact dermatitis

20
Q

DTH is important defense in

A

Intracellular pathogens like mycobacteriam fungi, and parasites

21
Q

T cell med cytotoxicity

A

CD8s kill antigen bearing target cells…primary allograft rejection mechanism
Granzyme induces apoptosis
Fas-fas ligand dependent killing can also cause apoptosis since FasL is on surface of CD8s