Hypersensitivity 3 and 4 Flashcards Preview

POD Exam II > Hypersensitivity 3 and 4 > Flashcards

Flashcards in Hypersensitivity 3 and 4 Deck (12):

Type III hypersensitivity:

Immune Complex Mediated Hypersensitivity
- Involves IgG or IgM antibodies that react with *soluble* antigens to form immune complexes that are deposited in tissues.
- Complement and Fc-mediated inflammation leads to tissue damage.
- Can be systemic or localized.


Deposition of immune complexes - favored sites (5):

1. Kidneys.
2. Joints.
3. Small vessels.
4. Heart.
5. Skin.


Type III hypersensitivity disease associations (6):

1. Serum sickness.
2. Drug reactions.
3. Rheumatic arthritis.
4. Systemic lupus erythematosus.
5. Post-streptococcal GN
6. Polyarteritis nodosum.


Serum sickness:

- Antigen-antibody complexes form in circulation and deposit in tissues.
- Complement levels in serum decrease due to activation.
- Eventually excess antibody limits formation of complexes.


Serum sickness clinical manifestations:

- Rash.
- Fever.
- Arthralgia or arthritis.
- 1-2 weeks after first exposure.


Drug reactions:

- A type of serum sickness caused by hypersensitivity to an IV injection of a drug.
- Particularly antibiotics.
- Caused by drug-specific immune complexes.
- Small drug molecules may serve as haptens that bind to serum proteins that then develop antibody response either to the hapten or the hapten-protein conjugate.


Rheumatoid arthritis:

Autoimmune disease characterized by chronically inflamed synovium.
- IgM which has specificity for determinants on the Fc portion of the pt's own IgG is called rheumatic factor and is deposited in joints.


Systemic lupus erythematosus:

- Chronic inflammatory disease targeting mainly joints, kidneys, heart, skin and lung.
- Autoantibodies to multiple nuclear antigens, including double-stranded DNA.
- Antigen/antibody complexes damage tissues by activating complement and by engaging Fc receptors on immune cells expressing these receptors.


Post-streptococcal glomerulonephritis:

- Associated with group A strep.
- Immune complexes deposit in the lipid bilayer of the glomerular basement membrane.
- Activation of the classical complement pathway leads to damage to the basement membrane.
- Abrupt onset of symptoms 1-4 weeks after infection.
- Dark or smokey colored urine.


Type IV hypersensitivity:

Delayed Type Hypersensitivity or T Cell-Mediated
- Initiated by antigen specific Th1 cells.
- T cells and macrophages are the major cellular mediators.
- Cytokines amplify and continue response.


Hallmarks of Type IV hypersensitivity (4):

1. Delay in time required for the reaction to develop to re-exposure to antigen.
2. The recruitment of macrophages as opposed to neutrophils.
3. Extensive tissue damage.
4. Associated with cytokines.


Diseases associated with Type IV hypersensitivity (6):

1. Contact dermatitis.
2. MS.
3. Type I diabetes.
4. Rheumatoid arthritis.
5. Graph rejection.
6. Tumor immunity.