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MOD 1 Exam 2 and 3 > Ch 6: Immunopathies (Part 2 - Hypersensitivity) > Flashcards

Ch 6: Immunopathies (Part 2 - Hypersensitivity) Flashcards

1
Q

What are the types of hypersensitivity reactions?

A

Type 1 = IgE-mediated hypersensitivity (allergies)

Type 2 = IgG-mediated cytotoxic

Type 3 = Immune-complex mediated

Type 4 = cell-mediated

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2
Q

What are the Type 1 hypersensitivity reactions?

A

Uticaria
Angioedema
Anaphylaxis

Seasonal allergies
Food allergies
Asthma

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3
Q

What is the process of a Type-1 hypersensitivity rxn?

A

DCs present Ag to T-cells
T cells differentials to TH2
B cells class switch to IgE
Mast bind IgE to FceRI - activation

Interleukins involved: 
IL-4 = class switching 
IL-5 = eosinophil activation
IL-13 = enhanced IgE production
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4
Q

What happens when mast cells are activated?

A

Degranulation = histamine

Release of:
vasoactive amines and lipid mediators (leukotrienes B/C/D, Prostaglandin D2, PAF) = early phase
cytokines = late phase

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5
Q

What presentation can be seen with an immediate response (early phase)?

A

Vasodilation
Vascular leakage
Smooth muscle spasm

Characterized by vasodilation, congestion, edema

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6
Q

What presentation can be seen with an late phase response?

A

Infiltration of tissues with eosinophils, basophils, neutrophils
Epithelial damage

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7
Q

What cell dominated last phase rxn?

A

Eosinophils

Mast cells are for immediate rxn

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8
Q

What is eosinophilic esophagitis?

A

Food Ag-driven disease of childhood

Recurrent dysphagia 
Weight loss (couldn't swallow effectively, hurts to swallow)
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9
Q

What is a Type 2 Hypersensitivity Rxn?

A

Rxn where abs directly react with Ag present on cell surface or ECM

Autoabs
Exogenous Ag bound to cell surface

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10
Q

What are the 3 mechanisms of Type 2 hypersensitivity rxns?

A

Opsonization and phagocytosis

Complement and fc receptor-mediated inflammation

Ab mediated cellular dysfunction

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11
Q

Describe opsonization and phagocytosis in Type 2 hypersensitivity. What disease can you get?

A

Opsonization leads to phagocytosis - or direct lysis in case of Antibody dependent cellular cytotoxicity

Basic mechanism = No cells = anemia and thrombocytopenia

Dz:
Autoimmune hemolytic anemia
Autoimmune thrombocytopenia purpura

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12
Q

Describe complement and Fc receptor mediated inflammation in Type 2 hypersensitivity. What disease can you get?

A

Basic mechanism = damaged tissue + inflammation

Streptococcal proteins that cross-react with myocardium

Dz:
Vasculitis caused by ANCA
Goodpasture syndrome
Acute rheumatic fever

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13
Q

Describe what happens with vasculitis caused by ANCA.

A

Target ag = Neutrophil granule proteins, released from activated neutrophils

MOD = neutrophil degranulation and inflammation

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14
Q

Describe what happens with Goodpasture syndrome.

A

Target ag = noncollagenous protein in basement membrane of kidney glomeruli and lung alveoli

MOD = complement and Fc mediated inflammation

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15
Q

Describe what happens with acute rheumatic fever.

A

Target Ag = streptococcal cell wall ag; ab cross reacts with myocardial ag

MOD = inflammation, macrophage activation

Acute and chronic forms

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16
Q

Describe Ab-mediated cellular dysfunction in Type 2 hypersensitivity. What disease can you get?

A

Basic mechanism = dysfunction due to receptor blockade

Disrupted endocrine and neural signaling

Dz:
Myasthenia Gravis
Graves Disease
Insulin-resistant diabetes

17
Q

Describe what happens with myasthenia gravis.

A

Target ag = acetylcholine receptor

MOD = Ab inhibits Ach biniding, down-modulates receptors

18
Q

Describe what happens with Graves disease.

A

Target Ag = TSH receptor

MOD = Ab-mediated stimulation of TSH receptor

19
Q

Describe what happens with insulin resistant DM.

A

Target Ag = Insulin receptor

MOD = Ab inhibits binding of insulin

20
Q

What is Type 3 Hypersensitivity Rxn? What is the mechanism?

A

Ag-Ab complexes form and deposit causing damage

Mechanism:
Ab combines with Ag
Circulating immune complexes lodged in basement membrane of epithelia (kidney, lungs, joints, skin)
Fragments of complement cause release of histamine and other mediator substances
Neutrophils migrate to site of immune complex and release enzyme that cause severe damage

21
Q

What type of diseases can you get with Type 3 hypersensitivity?

A

Serum sickness

Arthus reaction

22
Q

What is serum sickness?

A

Acute form classically due to non-human protein Ag (diphtheria antitoxin)

Chronic form usually due to self antigen (LUPUS)

23
Q

What is Arthus reaction?

A

It is a rare local effect of vaccination

Experimentally seen in rabbits inked with horse serum

24
Q

How would immunofluorescence on kidney biopsies look different on Type 2 and 3 hypersensitivity diseases?

A

Type 2 = smooth and linear

Type 3 = grainy and granular

25
Q

How do streptococcal proteins affect the heart and kidney differently?

A

Heart = cross-reactive Abs directly act on myocardium = Type 2

Kidney = cross-reactive abs are forming immune complexes that deposit in glomeruli = Type 3

26
Q

What is characteristic of Type 4 hypersensitivity? What are the 2 mechanisms?

A

Uses T-cells
CD4 response = cytokine release + inflammation
CD8 = cytotoxic against Ag on surface of target cell

2 Mech:
Cytokine mediated inflammation
T-cell mediated killing of host cells

27
Q

What is one hallmark of Type 4 hypersensitivity?

A

Immune granulomas = caused by variety of agents capable of inducing persistent T-cell mediated immune response

28
Q

What are some Type 4 Hypersensitivity diseases?

A 
Rheumatoid arthritis 
Multiple Sclerosis 
Type 1 DM
IBD
Psoriasis 
Contact sensitivity
29
Q

What is the tuberculin skin test?

A

A tuberculin purified protein derivative (PPD) us injected intradermally
48-72 hrs later, rxn assessed
Sensitized T cells start inflammatory response
Local swelling (induration) results
Indicated prior or current TB exposure

MOD 1 Exam 2 and 3 (9 decks)

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