Immunopathology Flashcards

1
Q

What is type II hypersensitivity?

A

Direct antibody binding to cells

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2
Q

What is type III hypersensitivity?

A

Deposition of antigen-antibody complexes

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3
Q

What is type IV hypersensitivity?

A

T lymphocytes and macrophage mediated hypersensitivity

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4
Q

Is IgE the only thing that can activate a mast cell?

A

No, a number of other molecules can activate a Mast cell

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5
Q

Describe the process of a Type I hypersensitivity reaction

A
  1. Antigen processed by DC
  2. Th2 is stimulated
  3. B cell+ antigen differentiates into plasma cell
  4. Plasma cell makes IgE
  5. IgE binds FcRe on mast cells
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6
Q

What are the two phases of type I reactions?

A

Immediate response: release of pre-formed mediators
Delayed response: Mast cell begins synthesis of other soluble mediators

The delayed response is more dangerous

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7
Q

What are the primary mediators?

A
  1. Biogenic amines
  2. chemotactic mediators
  3. enzymes
  4. Proteoglycans
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8
Q

What are the secondary mediators?

A

Leukotrienes
Prostaglandins
Platelet activating factor
Cytokines

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9
Q

What do eosinophil release?

A

Major basic protein (causes mast cell degranulation)
LTC4
Peroxidase Arylsulphylase
Platelet activating factor

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10
Q

What is severe urticaria

A

Cold/heat induced mast cell degranulation

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11
Q

What are the structural changes you will observe in a chronic asthmatic?

A
  1. Epithelial shedding
  2. Gland hyperplasia
  3. Basement membrane pseudothickening
  4. Muscle hyperplasia
  5. Inflammatory infiltrate
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12
Q

If incompatible blood types are mixed, what determines whether acute vs. delayed hemolysis will occur?

A

If previous exposure to different antibodies has occurred in the past, response will be acute. With no previous exposure, hemolysis will be delayed

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13
Q

Antiblood antibodies are typically what type of immunoglobulin?

A

IgM

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14
Q

What causes erythroblastosis fetalis?

A

When an Rh+ baby is born to an Rh- mother. This causes immunological attack on the baby’s erythrocytes. Baby responds by generating lots of erythroblasts, but eventually cannot compensate. Type II

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15
Q

What is goodpasture’s disease?

A

Anti-Type IV collagen antibody. Causes renal failure and hemoptysis Type II

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16
Q

What is rheumatic fever?

A

After streptococci infection, immunological attack of those same antibodies to self antigens of the heart. Causes heart valve vegetations, Aschoff bodies, and Anischkow bodies. Type II hypersensitivity

17
Q

What is grave’s disease?

A

Hyperthyroidism caused by antibodies to TSH receptors, causing constant stimulation of the thyroid gland

18
Q

What is responsible for causing most of the damage in Type III hypersensitivity reactions?

A

Neutrophils, which do most of the damage

19
Q

What is post-streptococcal glomerulonephritis? What type if hypersensitivity rxn is this?

A

Nodules of complexes form in basement membrane with a loss of neutrophils. PMNs enter glomerular tufts. Lumpy bumpy basement membrane. Type III.

20
Q

What is vasculitis?

A

Loss of smooth muscle with necrosis and thrombosis of vessels. Type III

21
Q

What is a type IV hypersensitivity reaction?

A

Attack of antigen-specific and sensitized T cells accompanied by macrophages

22
Q

What causes granulomatous formation?

A

A type IV hypersensitivity rxn that persists and becomes chronic

23
Q

What mediates a delayed type hypersensitivity rxn (type IV)?

A

CD4+ cells and macrophages

24
Q

What cells are responsible for T cell mediated cytotoxicity?

A

CD8+ cells

For tumors or viruses

25
Q

Which cells are responsible for organ rejection?

A

CD4+ and CD8+ cells

26
Q

What are the three types of rejections for organ transplants? What timeframe does each occur in?

A

Hyperacute rxn (0-48 hrs) resulting from preformed antibodies and rapid thrombosis

Acute rejection (week-months) Can be acute cellular (sensitized CD4 + CD8 cells, lymphocytes, macrophages) OR acute humoral=anti-graft antibodies

Chronic rejection (months-years) causing vasculitis, fibrosis of intima, thrombosis, organ ischemia, PMN infiltrate

27
Q

In graft rejection, what serves as the antigen?

A

The donor’s MHC molecule

28
Q

What is the direct pathway for graft rejection?

A

The donor’s APC presents to the host CD8+ and CD4+ cells

29
Q

What is the indirect pathway for graft rejection?

A

The recipient’s APC phagocytoses and presents to CD4+ cells