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Micro FINAL EXAM > Hypersensitivity - Stiener-jones > Flashcards

Hypersensitivity - Stiener-jones Flashcards

1
Q

What is hypersensitivity?

A

Exaggerated or aberrant immune response to antigen resulting in inflammation and tissue damage.

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2
Q

What is Type I hypersensitivity?

A

Referred to as Allergy, atopy or immediate hypersensitivity.

  • occurs mixtures after reexposure to antigen/allergen.
  • Rapid IgE and mast cell mediated vascular and smooth muscle reaction that is often followed by inflammation.
  • Affects 20% of population.
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3
Q

What is the basic sequence of events with Type I hypersensitivity?

A
  1. Initial exposure to antigen and production of IgE = Sensitization.
    - Th2 cells secrete IL’s
    - Th2 cell Cd40L binds to B cell Cd40
  2. Binding of IgE Ab to Fc receptor on mast cells
  3. Cross-linking of bound IgE upon reexposure to allergen.
  4. Release of mast cell mediators
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4
Q

What are the immediate effects of Type I Hypersensitivity?

A

Dilation of blood vessels, increased vascular permeability, smooth muscle contraction.

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5
Q

What is the late response of Type I hypersensitivity?

A

Inflammation

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6
Q

What are the common allergens, Route of entry and response of Systemic anaphylaxis?

A

Common allergens: Drugs, venoms, peanuts & serum.

Route of entry: Intravenously or oral absorption

Response: Edema, increased vascular permeability, Tracheal occlusion, circulatory collapse, death.

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7
Q

What are the common allergens, Route of entry and response of Acute urticaria?

A

Common allergens: Animal hair, insect bites, allergy testing

Route of entry: Through skin

Response: Local increase in blood flow and vascular permeability.

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8
Q

What are the common allergens, Route of entry and response of Allergic Rhinitis?

A

Common allergens: Pollens & dust mite feces

Route of entry: inhalation

Response: Edema & irration of nasal mucosa

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9
Q

What are the common allergens, Route of entry and response of Asthma?

A

Common allergens: Danders, pollens, dust mite feces

Route of entry: inhalation

Response: Bronchial constriction, increased mucous production and airway inflammation

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10
Q

What are the common allergens, Route of entry and response of Food allergy?

A

Common allergens: Tree nuts, peanuts, shellfish, milk, eggs, fish.

Route of entry: oral

Response: vomiting, diarrhea, purtisis, urticaria (hives), anaphylaxis.

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11
Q

What are the 2 lipid mediators?

A

Prostanglandins & Leukotrienes

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12
Q

What are the 2 lipid mediators?

A

Prostaglandins & Leukotrienes

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13
Q

What do Prostaglandins do?

A

*Made via cyclooxygenase pathway
VASOCONSTRICTION in the LUNGS or dilation in vascular smooth muscle.
- Cause aggregation or disaggregation of platelets.

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14
Q

What do Leukotrienes do?

A
  • Made in Lipoxygenase pathway
  • Powerful inducer of BRONCHOCONSTRICTION, INCREASED VASCULAR PERMEABILITY.
  • Refered to as slow reacting substance of anaphylaxis (SRS-A)
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15
Q

What are the 2 lipid mediators of mast cell Degranulation?

A

Prostaglandins & Leukotrienes

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16
Q

What is the immediate response of Mast Cell Degranulation?

A 
Vasoactive amines (Histamine and serotonin) and proteases.
- synthesis and secretions of lipid mediators (prostaglandins and Leukotrienes made from arachidonic acid)
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17
Q

What is the late–phase rxn of Mast cell Degranulation?

A
  • Synthesis and secretion of cytokines and chemokine.

- Infiltration of Eosinophils, monocytes and neutrophils.

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18
Q

What do ITAM’s do?

A

Activate map kinase

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19
Q

Map kinases are important in the formation of what?

A

Cytokines

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20
Q

What are the most common signs of asthma?

A

coughing, wheezing, shortness of breath

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21
Q

What causes the narrowing of airways with asthma?

A

Inflamed muscle wall.

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22
Q

Treatment strategies for asthma?

A
  • inhaled Corticosteroids (dampen inflammatory response)
  • Leukotriene modifiers (block chain of reaction)
  • Chromolyn =inhaled; prevents mast cell degranulation
  • Theophylline = opens airways.
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23
Q

Treatment strategies for asthma?

A
  • inhaled Corticosteroids (dampen inflammatory response)
  • inhaled long acting beta2 agonists = receive inflammation.
  • Leukotriene modifiers (block chain of reaction)
  • Chromolyn =inhaled; prevents mast cell degranulation
  • Theophylline = opens airways.
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24
Q

Intravenous antigen (gets into blood) causes what?

A

mast cell degranulation = systemic response = systemic anaphylaxis

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25
Q

Low does inhalation of antigen leads to what?

A

Hay fever symptoms

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26
Q

Low dose inhalation of antigen leads to what?

A

Hay fever symptoms

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27
Q

Enzymes released from mast cells cause what?

A

Tissue damgage

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28
Q

Cytokine & Lipid mediators released from mast cells cause what?

A

inflamation

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29
Q

Cytokine & Lipid mediators released from mast cells cause what?

A

inflammation

30
Q

All clinical and pathological features of immediate hypersensitivity reactions are driven by ________.

A

Mediators produced by mast cells.

31
Q

The most severe from of immediate hypersensitivity is _____.

A

Anaphylaxis

32
Q

What 3 events occur as a result of mast cell activation?

A
  1. mast cell degranulation
  2. Synthesis and secretion of lipid mediators
  3. Cytokine release
33
Q

What is Type II hypersensitivity?

A

Antibodies produced by the immune response that bind to antigens on our own cell surfaces.

  • primarily IgG and IgM isotypes.
  • Host Ab binds to foreign Antigen on cell surfaces or binds self antigen.
34
Q

Type II hypersensivity can activate complement resulting in _________.

A

Membrane attack complex formation.

35
Q

Type II hypersensivity can activate complement resulting in _________.

A

Membrane attack complex formation.

*Leads to destruction of cells, inflammation, or interfere with normal cellular function.

36
Q

What is the Target antigen, Mechanism of disease and clinical/pathological manifestations of Autoimmune hemolytic anemia?

A

Target antigen: Erythrocyte membrane proteins

Mechanism of disease: opsonization and phagocytosis of erythrocytes.

Clinical manifestations: Hemolysis, anemia

37
Q

What is the Target antigen, Mechanism of disease and clinical/pathological manifestations of Myasthenia

A

Target antigen: Acetylcholine receptor

Mechanism of disease: Ab inhibits acetylcholine binding, down modulate receptors.

Clinical manifestations: Muscle weakness, paralysis

38
Q

What is the Target antigen, Mechanism of disease and clinical/pathological manifestations of

A

Target antigen: Thyroid stimulating hormone receptor

Mechanism of disease: Ab-mediated stimulation of TSH receptors

Clinical manifestations: Hyperthyroidism

39
Q

Type II Hypersensitivity is also known as _____.

A

Cytotoxic Hypersensitivity

40
Q

What happens in Hemolytic disease of the Newborn?

A

Maternal Ab’s target fetal RBC’s for destruction.

41
Q

Type II Hypersensitivity is also known as _____.

A

Cytotoxic Hypersensitivity

  • Hemolytic newborn
  • hemolytic anemia
  • Blood transaction reaction
  • Graves disease
  • Myasthenia gravis
42
Q

What happens in Blood transfusion reactions?

A

Hose anti-blood group Ab’s target transfused RBC’s fro destruction

43
Q

What happens in Myasthenia Gravis?

A

At receptor Ab’s bind to block the Ach receptor

44
Q

What happens in Graves Disease?

A

TSH receptor Ab’s stimulate TSH Receptor to over produce TSH.

45
Q

What happens in Hemolytic anemia?

A

Auto-Ab’s are produced against self antigens on the surface of RBC’s. This triggers rapid destruction of RBC’s, leading to anemia.

46
Q

Tx of Hemolytic anemia?

A

Prednisone or blood transfusion

47
Q

Tx of Newborn Hemolytic disease?

A

anti-Rh Ab

48
Q

Tx of Graves Disease?

A

radioactive iodine, anti-thyroid drugs or thyroid removal.

49
Q

Tx of Myasthenia Gravis?

A

Cholinesterase inhibitors and corticosteroids

50
Q

Summarize Type II….

A

Host Ab binds foreign Ag on cell surfaces or binds self Ag.

*IgG

51
Q

What is Type III Hypersensitivity?

A

Ag-Ab complexes clump and despot in blood vessels or tissues attracting an acute inflammation response.

52
Q

What happens to larger aggregates in Type III?

A

they fix complements and are cleared from circulation by phagocytes.

53
Q

What do small complexes in Type III do?

A

deposit in vessels or tissue.

54
Q

What are examples of Type III?

A

Systemic lupus, Arthus reaction, serum sickness, lupus nephritis and rheumatoid arthritis.

55
Q

Type III occurs within ______ after exposure to antigen.

A

3-10 hours

56
Q

In Type III, immune complexes trigger inflammation via 3 mechanisms, what are they?

A
  1. Mast cell activation
  2. Macrophage release TNF-Alpha and IL-1 that induce inflammatory cascade.
  3. C3a, C4a and C5a
57
Q

The Arthus rx (type III) is triggered in the ____ by _____.

A

Skin by IgG

58
Q

What are the symptoms of Arthus?

A

Swelling, induration, severe pain, edema, hemorrhage, (gangrene in extreme cases)

59
Q

Tx of arthus?

A

anti-inflammatory agents

60
Q

Serum sickness is example of ________.

A

transient systemic immune complex-mediated syndrome.

61
Q

What causes serum sickness?

A

Injection of a foreign protein or proteins which leads to antibody response.

62
Q

Symptoms of serum sickness?

A

Fever, chills, rash, nephritis, lymphadenopathy.

63
Q

_____ is self limiting and follows kinetics of secondary Ab response.

A

Serum sickness (Type III)

64
Q

Most severe Type III hypersensitivity disease?

A

SLE = IgG Ab against ubiquitous self antigen in all nucleated cells.

Damage can lead to death.

65
Q

Type III summary?

A

Ag-Ab complexes clump and aggregate in or near blood vessels attracting an acute inflammatory reaction.

  • Primarily IgG (possibly IgM or IgE)
  • Immune complex
  • Ex. arthus, serum sickness & SLE
66
Q

Tx of lupus?

A

avoidance or anti-inflammatory agents

67
Q

Tx of serum sickness?

A

don’t get shots. (avoid anti-venom, antihistamines, corticosteroids)

68
Q

Tx of Arthus?

A

avoidance or anti-inflammatory agents

69
Q

Tx of lupus?

A

NSAID, corticosteroids, immunosuppressive agents.

70
Q

What is Type IV hypersensitivity?

A

Its a cell mediated reaction, mediated by Ag specific T cells which induce macrophage infiltration in a sensitized individual.

  • DTH response to injected ir absorbed Ab
  • 2-3 days
  • Ex. TB test, contact dermatitis, chronic asthma, crohn’s disease.
71
Q

Type IV is generally initiated by ____>

A

Happens (small molecules that must become bound to a larger carrier molecule in order illicit an immune response.

72
Q

Tb test is example of _______.

A

Type IV

Micro FINAL EXAM (14 decks)

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