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Anatomic And Molecular Pathology > Immunopathology II (H.R) > Flashcards

Immunopathology II (H.R) Flashcards

1
Q

What are hypersensitivity rxns❓

A

Here, an organism responds to a renewed contact with an antigen that it already knows and to which it is hypersensitive

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2
Q

Describe the 4 hypersensitivity rxns and their effectors using the Gell and Coombs classification

A

Type I
Description: Immediate rxn
Effector: IgE antibodies

Type II
Description: Cytotoxic rxn
Effector: IgG and IgM antibodies

Type III
Description: Immune complexes
Effector: IgG and IgM antibodies

Type IV
Description: Delayed rxn (48hrs)
Effector: T cells

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3
Q

What do Type I, II and III hypersensitivity rxns have in common❓

What is the mediator of Type IV hypersensitivity rxn❓

A
  1. Mediated by Antibodies/Plasma cells

2-6hrs after exposure

  1. T-cell and macrophages

24-36hrs after exposure

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4
Q

List the examples of allergens that can cause type I hypersensitivity rxns

A

Tree, grass, weed pollens

Cat/animal dander antigens

Dust/mite/fecal/pellet antigens

Mold spores

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5
Q

What makes individuals susceptible to Type I hypersensitivity rxn❓

A

The propensity to make strong Th2 responses and make IgE antibodies against allergens

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6
Q
  1. What are the other names for type I hypersensitivity rxn❓

2. What is it characterized by❓

A
  1. Anaphylactic rxn
    IgE allergy
    IgE hypersensitivity rxn
  2. IgE production
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7
Q

Describe the pathogenesis of Type I hypersensitivity rxn

A 
Allergen inhalation/ingestion/injection
⬇️
Production of local chemokines *eotaxin
⬇️
Recruitment of Th2 cells
⬇️
Th2 secrete cytokines that are responsible for hypersensitivity rxn

IL-4: produces IgE
IL-5: activates eosinophils
IL-13: secretes mucus
⬇️
IgE is implanted on FcR of mast cells and basophils
⬇️
Priming of mast cell occurs
⬇️
Cross linking of IgE Fc on surface of mast cells on 2nd exposure
⬇️
Mast cell is stimulated and releases all its products (degranulates)

*eotaxin recruits eosinophils

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8
Q

Describe the function of:

IL-4
IL-5
IL-13

In Type I hypersensitivity rxns

A

IL-4: stimulates B cells to undergo heavy-class switching to IgE

IL-5: activated eosinophils

IL-13: stimulates mucus secretion

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9
Q

In Type 1 hypersensitivity rxn, the complement system isn’t activated

True or false❓
Which other hypersensitivity rxn mimics this❓

A

True

Type II (ADCC)
Type IV H. R
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10
Q

List the cells that express FceRI (Fc portion of the E heavy chain on IgE)

A

Mast cells
Basophils
Eosinophils

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11
Q

What are the primary and secondary mediators of hypersensitivity rxns❓

What do they cause❓

A 
1. 
Primary mediators:
•Histamine 
•Serotonin 
•NCF, ECF
•Proteases

Cause:
•Vasodilation
•Bronchoconstriction

2. Secondary mediators:
•Leukotrienes 
•Prostaglandins 
•PAF
•Cytokines

Cause:
•Lead to inflammation

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12
Q

List the consequences of the mediators of Type I hypersensitivity rxn

A

⬆️vascular permeability

⬆️glandular secretion

Smooth muscle contraction

Edema

Inflammatory cell attraction

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13
Q

List the mediators that cause:

  1. Chemotaxis
  2. Vasoactivity
  3. Smooth muscle spasms

In type I hypersensitivity rxn

A

Chemotaxis:
LTB4
ECF
NCF

Vasoactivity:
Histamine 
PAF
LTC4, D4, E4
Neutral protease 
PGD2
Smooth muscle spasms:
Histamine 
LTC4, D4, E4
PG
PAF
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14
Q

Mention some important medical conditions that fall into Type I hypersensitivity rxns and their symptoms

A
  1. Penicillin/Bee sting allergy (systemic anaphylaxis)
Symptoms:
Acute asthma 
Laryngeal edema 
Diarrhea 
Urticaria 
Shock
  1. Food allergies/Allergic rhinitis/Hay fever (local anaphylaxis/atopy)

Symptoms:
Asthma
Hives

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15
Q
  1. What are the other names for type II hypersensitivity rxn❓
  2. What is it characterized by❓
A

Cytotoxic rxn

IgG/IgM immunoglobulins

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16
Q

Describe the pathogenesis of Type II hypersensitivity rxn

A 
•Complement-dependent cytotoxicity:
Ag/Ab rxn 
⬇️
Complement pathway (classical pathway) is activated
⬇️
Cell lysis

eg Transfusion rxns
Autoimmune hemolytic anemia
Erythroblastosis fetalis
Goodpasture’s syndrome

•Antibody-dependent cell-mediated cytotoxicity:
Low conc of IgG/IgE (parasitic) coat target cells
⬇️
Inflammatory cells bind to FcE receptors
⬇️
Cell lysis
🚫phagocytosis

Eg Transplant rejection
Immune rxns against neoplasms/parasites

•Anti-receptor antibodies:
IgG antibody is directed against receptors in target cells
⬇️
Complement-mediated destruction of the receptors
⬇️
Functional derangement
🚫cell injury

Eg Mysthenia graves (anti ACh receptor)
Graves’ disease (anti TSH receptor/TSI)
Pernicious anemia

17
Q
  1. What are the other names for type III hypersensitivity rxn❓
  2. What is it characterized by❓
A
  1. Immune complexes

2. Ag-Ab complexes

18
Q

Describe the pathogenesis of Type III hypersensitivity rxn

A 
⬆️Circulating, soluble immune complexes containing IgG/IgM antibody 
⬇️
Deposition in tissues
🚫removal by mononuclear phagocytes 
⬇️
Activation of complement

*C3b and C5a attracts neutrophils and are used up

19
Q

Is serum complement increased or reduced in:

  1. Complement-dependent, Type II H.R
  2. Immune complex, Type III H. R
A
  1. Serum complement ⬆️ in type II complement dependent H. R

2. Serum complement ⬇️ in type III H. R

20
Q

Which H. R is sometimes classified as TYPE V❓

A

Antireceptor antibodies, Type II H. R

21
Q

What are the differences between Complement-dependent (Type II H.R) and Immune complex (Type III H. R)❓

A
  1. Serum complement ⬆️ in type II complement dependent H. R

Serum complement ⬇️ in type III H. R

  1. The Ag is not an intrinsic component of the target cells in Type III H. R
22
Q

Mention some important medical conditions that fall into Type III hypersensitivity rxns

A

Systemic immune complex:
Glomerulonephritis
Serum sickness
Vasculitis

Local immune complex/Arthus rxn:
Pneumonitis/Farmers lung

SLE
Polyarteritis nodosa
Rheumatoid arthritis 
Lupus nephropathy
Post-streptococcal GNs
23
Q

What is Arthus rxn❓

A 
Injection/local transplant of antigen in the presence of preformed Ab
⬇️
Ag-Ab binding 
⬇️
Formation of immune complexes locally 
⬇️
Precipitation in vessel walls 
⬇️
Fibrinoid necrosis and thrombosis
⬇️
Ischemic injury
24
Q

What is Serum Sickness❓

A

Systemic deposition of Ag-Ab complexes in multiple sites (esp kidneys, heart, joints)

25
Q

What are the three phases of systemic immune complex disease❓

A
  1. Formation of Ag-Ab complexes in the circulation
  2. Deposition in various tissues
  3. Inflammatory rxn
26
Q

What is the striking characteristic of SLE❓

A

Malar rash-immune complex deposition

27
Q

What happens in PAN❓

A

Generalized immune complex disease involving small and medium sized arteries

28
Q
  1. What are the other names for type IV hypersensitivity rxn❓
  2. What is it characterized by❓
A
  1. Mediated/Delated Type
  2. T-cell and macrophage mediated
    🚫antibody
    🚫complement system
29
Q

Describe the pathophysiology of Type IV, Delayed-type and Immune inflammation H. R

A

Display of peptides by APCs (dendritic cells)

Production of cytokines by APCs*
Production of IL-2 by APCs**
Production of IL-1, 6, 23 by APCs***
⬇️
Recognition by naive CD4+ cells 
⬇️
Secretion of IL-2
⬇️
Proliferation of T cells 
Differentiation to Th1/Th17*
Differentiation of CD4+ T cells to Th1 subset**
Differentiation to Th17***
⬇️
Repeated exposure to antigen
⬇️
Th1 secretes IFN-gamma 
⬇️
Inflammation
Phagocytosis 
⬇️
Removal of offending agent
30
Q

Rxn of CD4+ T cells are seen in delayed type H.R and immune inflammation

True or false❓
Which cells are involved in cell-mediated cytotoxicity❓

A

True

CD8+ T cells

31
Q

In Type IV H. R, Th17 cells secrete which cytokines❓

A

IL-17
IL-21 (amplifies Th17 response)
IL-22

32
Q

The tuberculin rxn is a type of DTH (Type IV), what happens in this rxn❓

A

Intracutaneous injection of purified protein derivative/tuberculin
⬇️
Accumulation of CD4+ T cells and macrophages around venules (perivascular cuffing)
⬇️
Cytokine-mediated endothelial activation
⬇️
Macrophages become epithelioid cells/granuloma

Reddening and induration of site 8-12 hrs

Peaks 24-72 hrs

Subsides

33
Q

Contact dermatitis is evoked by contact with urushiol (antigenic component of poison ivy or poison oak)

True or false

A

True

34
Q

Describe the pathophysiology of Type IV, Cell-Mediated H. R

A

Th1 cells recognize antigenic peptide on APC

Secrete IFN-gamma (inflammatory rxns)

CD8+ CTLs kill antigen-bearing target cells

Fas ligand (apoptosis)

Perforins, granzymes and serglycin (enter through endocytosis)

Perforin facilitates the release of granzymes from the complex

Granzymes cleave and activate caspases which cause apoptosis of target cells

35
Q

Antibodies and complement play no role in Delayed type H. R

True or false

A

True

36
Q

Mention some important medical conditions that fall into Type IV, Cell-Mediated hypersensitivity rxns

A

Granuloma diseases (mycobacteria, fungi)

Tuberculin skin rxns

Contact dermatitis

Tumor rejection

Graft rejection

Type 1 diabetes

Reactions against viruses

37
Q

What are the the substances that could trigger contact dermatitis❓

A

Poison ivy (catechols)

Nickel

Formaldehyde

Latex

Chromium

Dyes in clothing and cosmetics

38
Q

In CTL (Cytotoxic T-lymphocyte mediated responses),

  1. Class I HLA molecules play a role
  2. Cytokines are not involved

True or false
Rxns with this mode include

A

True

Neoplasia cell lysis
Transplant rejection
Virus-infected cell lysis

Anatomic And Molecular Pathology (14 decks)

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