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SFM Exam 2 > 17: Hypersensitivity > Flashcards

17: Hypersensitivity Flashcards

1
Q

Type I hypersensitivity: primary exposure to allergen: 5 Steps

A
  1. Th2 cell activation (via IL-4)
  2. B cell activation
  3. IgE production
  4. IgE binds FCER (CD23) on mast cells
  5. Pt now sensitized to allergen
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2
Q

Type I hypersensitivity: subsequent allergen exposures: 2 Steps

A
  1. Ag cross-linking of IgE on mast cells -> mast cell activation
  2. Mast cells release inflammatory mediators
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3
Q

Atopy

A

Genetic tendency to develop allergic disease

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4
Q

Five inflammatory mediators released by mast cells

A

Cytokines, histamine, proteases, prostaglandins, leukotrienes

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5
Q

Immediate vs late phase reaction of type I hypersensitivity

A

Immediate: within minutes - vasodilation and edema

Late phase: 2-24hrs later - inflammatory infiltrate rich in eosiniohils, neutrophils, and T cells

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6
Q

Three examples of type I hypersensitivities

A
  1. Allergies
  2. Asthma
  3. Anaphylaxis
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7
Q

Three major mediators of asthma

A

Mast cells, prostaglandins, leukotrienes

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8
Q

Asthma vs anaphylaxis

A

Asthma: local reaction
Anaphylaxis: systemic

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9
Q

Two cell types involved in anaphylaxis

A

Mast cells, basophils

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10
Q

3 goals of allergen-SIT

A
  1. Induce peripheral T cell tolerance by generating Tregs
  2. Increase threshold for mast cell and basophil activation by allergens
  3. Decrease IgE-mediated histamine release
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11
Q

Type II hypersensitivity

A

Abs bind tissue Ags -> cause complement dependent tissue injury

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12
Q

What cells release inflammatory mediators in type II hypersensitivity

A

Neutrophils and macrophages

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13
Q

11 Examples of Type II Hypersensitivity

A
  1. ABO blood transfusion reaction
  2. Hemolytic disease of Newborn
  3. Drug-induced hemolytic anemia
  4. Autoimmune hemolytic anemia
  5. Autoimmune thrombocytopenic purpura
  6. Goodpastures syndrome
  7. Graves’ disease
  8. Myasthenia gravis
  9. Pemphigus vulgaris
  10. Pernicious anemia
  11. Rheumatic fever
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14
Q

How do we form Abs against blood group Ags that we dont have?

A

There are sugars that are identical (or v similar) to blood group Ags in foods or microbes, which we form reactions to to produce Abs

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15
Q

Hemolytic disease of newborn

A

The Rh thing

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16
Q

Three types of drug-induced hemolytic anemia and treatment used

A
  1. Penicillin: no tx needed
  2. Quinidine: immunosuppression/plasmapheresis
  3. Methyldopa: same as quinidine
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17
Q

What is targeted in autoimmune thrombocytopenic purpura?

A

Platelet membrane proteins

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18
Q

What is targeted in goodpastures syndrome?

A

Proteins in kidney glomeruli and lung alveoli

19
Q

Grave’s disease

A

Ab-mediated stimulation of TSH receptors

20
Q

Myasthenia gravis

A

Ab inhibits Ach receptor, causing muscle weakness, paralysis, and ptosis

21
Q

Pemphigus vulgaris

A

Abs target intercellular epidermal junctions -> vesicles on skin

22
Q

Pernicious anemia

A

Ab neutralizes intrinsic factor -> decreased vitamin B12 absorption

23
Q

Rheumatic fever

A

Ab targets strep cell wall, which cross-reacts with myocardial Ags

24
Q

Type III hypersensitivity

A

Circulating/soluble ICs form -> deposit in vessels -> complement activation

25
Q

Five examples of type III hypersensitivity

A
  1. SLE
  2. Polyarteritis nodosa
  3. Post-strep glomerulonephritis
  4. Serum sickness
  5. Arthus reaction
26
Q

SLE Ab specificity

A

Ab specific for DNA or nucleoproteins

27
Q

Polyarteritis nodosa

A

Ab specific for microbial agents -> vasculitis

28
Q

Post strep glomerulonephritis

A

Ab specific for strep cell wall Ag -> nephritis

29
Q

Serum sickness and arthus reaction specificity

A

Ab specific for various protein Ags

30
Q

Serum sickness vs arthus reaction

A

Serum sickness: systemic + clinical or experimental

Arthus: local + experimental

31
Q

Serum sickness

A

Antiserum injected into blood -> Fc receptors on endothelium bind antitoxin Ab that has reacted with toxoid -> complement activation

32
Q

Arthus reaction

A

SubQ administration of protein Ag to a previously immunized animal -> IC formation at injection site -> vasculitis and complement cascade

33
Q

When do type IV hypersensitivities develop?

A

24-48 hours after Ag exposure

34
Q

Four major cell players in type IV hypersensitivity

A

Th1, Th17, CTLs, macrophages

35
Q

Six examples of type IV hypersensitivity

A
  1. MS
  2. RA
  3. DM I
  4. IBD / Crohn’s
  5. Chronic infection
  6. Contact dermatitis / sensitivity
36
Q

MS

A

T cells target myelin proteins -> demyelination in CNS

37
Q

RA

A

T cells target Ags in joints

38
Q

DM I

A

T cells target pancreatic islet Ags

39
Q

Crohn’s and IBD

A

T cells target unknown Ag linked to intestinal microbes

40
Q

Chronic infection

A

T cells target microbial infection -> chronic inflammation

41
Q

Contact sensitivity / dermatitis

A

T cells target modified skin proteins

42
Q

Most common contact allergen

A

Metals

43
Q

PPD

A

Purified protein derivative: protein Ag of mycobacterium tuberculosis that elicits a DTH reaction called tuberculin reaction in previously infected individuals

SFM Exam 2 (19 decks)

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