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BIOC 372: Immunology > L15: Hypersensitivity > Flashcards

L15: Hypersensitivity Flashcards

1
Q

Agent and symptoms of Type I hypersensitivity:

A

IgE

itching, rash, anaphylactic shock

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2
Q

Agent and symptoms of Type II hypersensitivity:

A

IgM, IgG

massive hemolysis, anemia, kidney failure

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3
Q

Agent and symptoms of Type III hypersensitivity:

A

IgG

serum sickness, kidney failure

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4
Q

Agent and symptoms of Type IV hypersensitivity:

A

TDTH, TH1, TC, macrophages

contact dermatitis

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5
Q

Activation of adenyl cyclase produces:

A

cAMP

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6
Q

Activation of phospholipase C produces:

A

DAG and PIP2

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7
Q

The release of Ca2+ from the ER has several effects:

A

a. synthesis of prostaglandins and leukotrienes
b. assembly of microtubules and microfilaments at the cortex
c. fusion of granule (vesicle) with the plasma membrane.

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8
Q

How do you trigger degranulation?

A

Cross-linking two high affinity receptors bound to the Fc of the IgE with an allergen activates the tyrosine kinases associated on the cytoplasmic sid

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9
Q

What’s released in degranulation?

A
  • Histamine
  • prostaglandins
  • luekotrienes
  • cytokines
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10
Q

Histamine

A
  • increases smooth muscle contraction of intestine and bronchioles
  • increases permeability of venules
  • increases mucus secretion by goblet cells
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11
Q

prostaglandins

A
  • synthesized after granule release from arachandoic acid

- bronchoconstrictor

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12
Q

leukotrienes

A
  • synthesized after granule release from arachandoic acid

- does everything histamine does only more strongly and longer

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13
Q

cytokines

A
  • promote inflammatory responses by eosinophils and neutrophils
  • TNF-α may also induce shock.
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14
Q

Type I clinical conditions include:

A
  • anaphylactic shock
  • Allergic rhinitis
  • food allergies
  • asthma
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15
Q

How does epinephrine work?

A

reduces vascular permeability, relaxes smooth muscles, increase cardiac output, and raises cAMP levels, blocks further degranulation.

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16
Q

Type II clinical conditions include:

A
  • Blood transfusion mismatches
  • Rh incompatibility
  • drug-induced hemolytic anemia
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17
Q

Type III clinical conditions include:

A
  • caused by build up of antigen-antibody complexes
  • arthritis
  • kidney damage
  • clotting
  • serum sickness
  • autoimmune diseases
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18
Q

Type IV clinical conditions include:

A
  • granulomas (like in TB and leprosy)
  • contact dermatitis
  • graft rejection
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19
Q

Novotny description of Type I:

A

classical allergy

20
Q

Novotny description of Type II:

A

Antibodies target cells for ADCC

21
Q

Novotny description of Type III:

A

Excess antibody-antigen complexes

22
Q

Novotny description of Type IV:

A

Immune cells target rogue cells

23
Q

Subsequent response time (once sensitized)-Type I

A

immediate

24
Q

Subsequent response time (once sensitized)-Type II

A

immediate

25
Q

Subsequent response time (once sensitized)-Type III

A

immediate

26
Q

Subsequent response time (once sensitized)-Type IV

A

1-3 days

27
Q

mechanism-Type I

A

IgE activates mast cells and basophils

28
Q

mechanism-Type II

A

IgM and IgG attach to cells, attracting non-specific cytotoxic cells

29
Q

mechanism-Type III

A

IgG-antibody complexes overwhelm phagocytosis, triggering excess inflammation

30
Q

mechanism-Type IV

A

TDTH cells (a type of TH1) signal with cytokines to attack self cells with intracellular pathogen

31
Q

Cells involved-Type I

A

Mast cells, basophils, and then responding eosinophils

32
Q

Cells involved-Type II

A

NK cells, macrophages, and neutrophils

33
Q

Cells involved-Type III

A

neutrophils

34
Q

Cells involved-Type IV

A

macrophages and TC cells (not neutrophils)

35
Q

Pathology results from-Type I

A

Substances released by degranulation –smooth muscle

contraction

36
Q

Pathology results from-Type II

A

Attack on the marked cells by the cytotoxic cells and complement. Red blood cells especially sensitive

37
Q

Pathology results from-Type III

A

Clumps of complexes activating complement, releasing anaphylatoxins; damage by neutrophils

38
Q

Pathology results from-Type IV

A

Excess damage to healthy tissues by macrophages and TC cells

39
Q

Diseases- Type I

A

Hay fever, hives, eczema, food allergies, asthma,

shock

40
Q

Diseases- Type II

A

Transfusion reactions, erythroblastosis fetalis, hemolytic anemia

41
Q

Diseases- Type III

A

Local – response to insect bites (Arthus), lung irritants. Systemic: serum sickness, kidney damage

42
Q

Diseases- Type IV

A

Contact dermatitis, formation of granulomas, graft rejection

43
Q

Related factoids- Type I

A

Less likely to occur in people exposed to

farm animals

44
Q

Related factoids- Type II

A

Hemolysis leads to kidney damage

45
Q

Related factoids- Type III

A

autoimmune disorders(SLE) leading to excess of complexes may trigger this

46
Q

Related factoids- Type IV

A

Basis of skin test for tuberculosis

BIOC 372: Immunology (22 decks)

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