Week 3 (Part 2): Hypersensitivity II, III, IV Flashcards

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1
Q

Type II antibody-mediated hypersensitivity reactions are mediated by…

A

… IgG or IgM antibodies directed against target antigens on cell surfaces

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2
Q

Type II anti-body mediated hypersensitivity antigens can be endogenous or exogenous?

A

Both

  • Endogenous: antigens that are present on the membranes of body cells
  • Exogenous: antigens that are absorbed on the membrane surface
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3
Q

Type II anti-body mediated hypersensitivity - The reaction destroys the antigen in one of the following ways (3):

A
  1. Opsonization and phagocytosis – cells are coated (opsonized) with molecules that make them attractive to phagocytes
  2. Anti-body dependent cellular toxicity, where IgG binds to the surface antigen on the infected cell, the NK cell then recognizes it and kills the antibody coated infected cell
  3. Complement activation: the binding of a IgG to an antigen can activate the complement system and cause lysis of the antigen by membrane attack complex or by phagocytosis.
    - Complement activation generates the recruitment of neutrophils and monocytes which release injurious substances like specific enzymes, and this results in inflammation and tissue damage
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4
Q

What is Rh incompatibility?

A

Rh incompatibility is a condition that occurs during pregnancy if a woman has Rh-negative blood and her baby has Rh-positive blood.

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5
Q

What is Rh factor?

  • If you have it?
  • If you don’t have it?
  • Inherited how?
  • Majority of people?
A

Rh factor is a protein on red blood cells.

  • If you have Rh factor, you’re Rh-positive.
  • If you don’t have it, you’re Rh-negative.
  • Rh factor is inherited (passed from parents to children through the genes).
  • Most people are Rh-positive.
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6
Q

When can blood from the baby cross into the blood stream of the mom?
- Especially during?

A

In pregnancy blood from the baby can cross into the bloodstream of the mom
- especially during delivery

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7
Q

If mom is Rh-negative and baby is Rh-positive, the mom’s body will react to the baby’s blood as a foreign substance

  • What does the body create?
  • Do they cause problems? Why or why not?
A

The body will create antibodies against the baby’s Rh-positive blood.

These antibodies usually don’t cause problems during a first pregnancy.
This is because the baby often is born before many of the antibodies develop.

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8
Q

Why is Rh incompatibility is more likely to cause problems in second or later pregnancies (if the baby is Rh-positive)?

A

The antibodies stay in the mom’s body once they have formed.

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9
Q

The Rh antibodies can cross the placenta and attack the baby’s red blood cells, what can this cause?

A

This can lead tohemolytic anemia in the baby.

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10
Q

What do we give pregnant women to prevent Rh antibody formation?

A

This is why we give all pregnant women who are Rh negative Rhogam, and immunoglobulin to prevent antibody formation against the baby’s foreign antigen

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11
Q

What are hypersensitivity type III reactions mediated by?

  • activates?
  • produces?
A

Mediated by the formation of insoluble antigen-antibody complexes

  • activates the complement system
  • produces localized inflammation
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12
Q

In hypersensitivity type III reactions where are immune complexed formed?
- Wat occurs once deposited?

A

Immune complexes formed in the circulation produce damage when they come in contact with the vessel lining or are deposited in tissues.
- Once deposited the immune complexes elicit an inflammatory response by activating complement, leading to recruitment of neutrophils and other inflammatory cells, this activation is directly responsible for injury that occurs to the affected tissue

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13
Q

What are type III reactions responsible for seen in certain immune disorders?

A

Type III reactions are responsible for the vasculitis seen in certain autoimmune disorders such as SLE (lupus) or kidney damage seen in acute glomerulonephritis (such as post-strep infections)

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14
Q

What is Poststreptococcal glomerulonephritis (PSGN) is characterized by?
- What does this condition result from?

A
Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) followingstreptococcal infection. 
- This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci.
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15
Q

What does Poststreptococcal glomerulonephritis (PSGN) affect?

A

The disease affects the glomeruli and the small blood vessels of the kidneys.

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16
Q

When does PSGN most frequently presents?

A

PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo)

17
Q

What is the mechanism of PSGN?

A

The exact mechanism by which PSGN occurs is not fully determined.

  • The body responds to nephrogenic streptococcal infection by forming immune complexes containing the streptococcal antigen with a human antibody.
  • Some theories suggest that these immune complexes become deposited in kidney glomeruli reaching through the circulation.
  • Others claim that the condition results from an “in situ” formation of the antigen-antibody complex within the kidney glomeruli.
18
Q

The presence of immune complexes leads to the activation of…
- Reduction of GFR can lead to?

A

… alternate complement pathway causing infiltration of the leukocytes, and proliferation of the other cells in the glomerulus thus impairing the capillary perfusion and glomerular filtration rate (GFR).
- Reduction in GFR can lead to renal failure (oliguria or anuria), acid-base imbalance, electrolyte abnormalities, volume overload, edema, and hypertension

19
Q

The classic triad of glomerulonephritis includes:

A

The classic triad of glomerulonephritis includes hematuria, edema, and hypertension.

20
Q

What is type IV hypersensitivity?

  • What does there need to be in order to mount an immune response?
  • Example
A

Type IV hypersensitivity reactions involve cell-mediated rather than antibody mediated immune responses, specifically and immune reaction in which T cells are activate by antigens
- There has to be a previous exposure to the antigen in the persons history in order to mount an immune response to a second exposure.

Ie) most people will not have a reaction to their first contact with poison ivy, but on a subsequent exposure (because they have been sensitized) they will then manifest the contact dermatitis associated with the antigen

21
Q

What is (DTH) is delayed-type hypersensitivity?

A

Type IV hypersensitivity

22
Q

One of the best known DTH responses is the reaction to the tuberculin skin test, how is the test done?

A

inactivated tuberculin is injected intradermally under the skin

  • In a person who has been sensitized by previous exposure to the infection, a local area of redness and induration develops within 8-12 hours, reaching a peak in 24-72 hours after a TB skin test.
  • The tuberculin reaction is characterized by perivascular accumulation of CD4 T cells and to a lesser extent macrophages. - Local secretion of cytokines by the cells lead to increased microvascular permeability with local redness and swelling