• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle 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

image

PLAY BUTTON

image

PLAY BUTTON

image

Progress

1/19

Click to flip

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