- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
![]()
PLAY BUTTON
![]()
PLAY BUTTON
![]()
19 Cards in this Set
- Front
- Back
|
What kind of immune reaction is a type II hypersensitivity response?
|
Cytotoxic
|
|
What causes type II hypersensitivity reactions?
|
Antibodies bind to antigens
- On cells - On extracellular components Cause damage |
|
What specific antibodies mediate type II hypersensitivity reactions and why?
|
IgM
IgG These trigger damaging effector mechanisms |
|
What are the ways in which antibody can cause damage and which antibodies are specific to these mechanisms?
|
Complement-mediated cytotoxicicty
- IgM - Some IgG Opsonization-causing phagocytosis - Complement and IgG Antibody-dependent cell-mediated cytotoxicity (ADCC) - IgG Antibody-mediated cellular dysfunction |
|
What are the two most important RBC antigens, what kind of antigens are they, and from where do they arise?
|
ABO
- Pre-existing IgM antibodies RhD - IgG stimulated by previous exposure to foreign RBCs (transfusion, pregnancy) |
|
How does the activation of complement differ between IgM and IgG?
|
IgM
- Pentamer that can directly activate pentameric C1 IgG - C1 needs two adjacent IgG to bind and activate |
|
Why is complement more effective against bacteria than mammalian cells?
|
Mammalian cells have surface proteins that inactivate deposited complement
Mammalian nucleated cells can repair complement damage to the membrane Bacteria lack these mechanisms |
|
Why are RBCs particularly sensitive to complement?
|
Lack complement regulatory proteins to inactivate complement
Lack nuclei to repair complement damage to membrane |
|
Describe the mechanism of phagocytosis-causing opsonization
|
1. Complement / IgG (both opsonins) bind and lead to opsonization of antigen
2. Antigen engulfed and killed by phagocytes |
|
Describe the mechanism of antibody-dependent cell-mediated cytotoxicity (ADCC)
|
IgG targets Fc receptors on macrophages and NK cells
Leads to phagocytosis |
|
Describe the pathophysiological mechanism of Rh incompatibility
|
Rh- mother with Rh+ fetus
1. First pregnancy/abortion causes immunization of mother with anti-Rh antibodies 2. Second pregnancy leads to IgG anti-Rh antibodies crossing placenta to fetal circulation 3. IgG antibodies bind fetal RBCs and cause opsonization and phagocytosis via antibody-dependent cell-mediated cytotoxicity (ADCC) |
|
What causes drug-induced hemolytic anemia?
|
Antibodies made against drugs that either
- Bind RBCs - Modify RBC antigens |
|
Rheumatic heart disease:
- Agent - Pathophysiology |
Agent
- β-hemolytic streptococcus Pathophysiology - Antibody made against β-hemolytic streptococcus - Cross reacts and deposits on basement membranes of heart valves and joints - Activates effector mechanisms |
|
Goodpasture's syndrome:
- Agent - Pathophysiology |
Agent
- Unknown Pathophysiology - Autoantibodies to type IV collagen made - Autoantibodies bind basement membrane in lung and kidney, activating effector mechanisms and leading to damage |
|
What is the pathophysiological mechanism of pemphigus vulgaris?
|
Autoantibody made to skin basement membrane leading to effector mechanisms and blistering disease
|
|
How do antibodies bound to extracellular antigens cause tissue damage?
|
Antibody and complement recruit and activate leukocytes, causing damage
|
|
What components of the complement cascade are proinflammatory and how do they do this?
|
C3a, C5a
Activate mast cell degranulation Chemoattract eosinophils, neutrophils, macrophages |
|
To what extent are extracellular components reactive to complement and why?
|
Very susceptible to complement
Lack regulatory components to inactivate complement |
|
Describe antibody-dependent cell-mediated cytotoxicity (ADCC) (mechanism)
|
1. Antibody binds antigen on cell / matrix
2. Effector cells bind antibody Fc receptors - Neutrophils - Macrophages - NK cells 3. Crosslinking FcR stimulates effector cells |