Immunopathology Flashcards

(29 cards)

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
Which cells are responsible for organ rejection?
CD4+ and CD8+ cells
26
What are the three types of rejections for organ transplants? What timeframe does each occur in?
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
In graft rejection, what serves as the antigen?
The donor's MHC molecule
28
What is the direct pathway for graft rejection?
The donor's APC presents to the host CD8+ and CD4+ cells
29
What is the indirect pathway for graft rejection?
The recipient's APC phagocytoses and presents to CD4+ cells