Hypersensitivity Flashcards

1
Q

How are hypersensitivity reactions able to arise?

A
  1. uncontrolled responses to foreign Ags

2. Autoimmune responses against self Ags

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2
Q

Describe Type 1 hypersensitivity

A

Immediate; caused by the release of mediators from mast cells (histamine, proteases, prostaglandins, leukotrienes, and cytokines)

-response to Environment in an allergic response (Th2)

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3
Q

Define atopy

A

tendency to develop allergies

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4
Q

Describe the primary encounter with the allergen (initial)

A

Allergen is inhaled, ingested, injected or contacted

B cells pick up the allergen and take it to the T cells, where they are formed into IgE secreting plasma cells

This IgE that is formed goes and binds to FcERI on the surface of mast cells waiting for the next exposure

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5
Q

Describe the subsequent allergen exposure (second) and what happens

A

allergen comes in contact with the mast cells who freak out and release all of the mediators resulting in vascular and smooth muscle contraction (vasoactive amines, prostaglandins, leukotrienes, and histamine), Endothelial vasodilation (histamine, prostaglandins), and leukocyte and chemotaxis activation (cytokines)

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6
Q

Differentiate between the immediate and late phases of a response to an allergen

A

Immediate:
-vascular and smooth muscle; vasodilation, congestion and edema

Late:
-inflammatory infiltrate of eosinophils, neutrophils, and T cells

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7
Q

Describe asthma

A

Reversible airway obstruction that is caused by an allergen- causes an inflammatory response including

increased capillary permeability, spasmodic contraction of smooth muscle around the bronchi (leading to SOB)

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8
Q

Describe anaphylaxis

A

exposure to an allergen causes a massive release of vasoactive amines and cytokines leading to extreme smooth muscle contraction and vasodilation

This leads to blood pressure drop and vascular shock

smooth muscle contraction leads to the contraction of the airway muscles, which makes breathing difficult

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9
Q

Describe allergen testing

A

tests type 1 hypersensitivities on the arm or the back with standardized allergens that are injected into the dermis; positive reactions result in redness and swelling

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10
Q

What are the aims of Allergen-SIT?

A
  • induce T cell tolerance
  • increase the thresholds for mast cell and basophil activation
  • decrease IgE mediated histamine release

To generate FOXP3+CD4+CD@%_ Treg cells

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11
Q

Describe Type II Hypersensitivity

A

Disease caused by Abs to Cell or tissue Ags which causes local inflammation

  • IgG and IgM activate the CP of the complement, which leads to increased C3a and C5a, leading to inflammation
  • Abs go to the FcRy or CR1 receptors which lead to the increase of the release of ROS and lysosomal enzymes, which will cause inflammation to the tissues
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12
Q

How are Abs able to cause diseases such as

  1. Graves disease
  2. Myasthenia graves
A
  1. Abs stimulate the activity of the thyroid stimulating hormone receptors causing hyperthyroidism
  2. Abs inhibit ACH from binding to the receptor
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13
Q

Describe a penicillin induced anemia

A

drug binds to the erythrocyte surface and induces and anti-drug Ab

improves when the drug is stopped

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14
Q

Describe a quinidine induced anemia

A

autoAbs form complexes with the drug

immune complexes can bind to the surface through CR1

treatment: immunosuppression and plasmaohoresis to remove the complexes

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15
Q

Describe a methyldopa induced anemia

A

Induces and anti-drug Ab that cross react with an rh antigen

treatment: immunosuppression and plasmapharesis

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16
Q

What are the type 2 hypersensitivity diseases?

A
  • autoimmune hemolytic anemia
  • Autoimmune thrombocytopenia purpuratus
  • Goodpastures syndrome
  • myasthenia gravis
  • pemphigus vulgaris
  • pernicious anemia
  • rheumatic fever
17
Q

Describe Type III Sensitivity

A

Diseases mediated by immune complexes of circulating antigens and IgM or IgG Abs that are deposited in I the vascular basement membrane

Ab-Ag immune complexes may be formed in circulation and deposited in blood vessels, kidneys, or lungs; major mechanism triggering tissue damage is the CP of complement activation and recruitment of leukocytes

18
Q

What are the diseases of Type III Hypersensitivity?

A
  • SLE
  • Polyarteritis nodosa
  • Post-streptococcal glomerulonephritis
  • Serum sickness (clinical and experimental)
  • Arthus reaction (experimental)
19
Q

Describe Type IV Hypersensitivity

A

Diseases mediated by T cells; CD4+ are cytokine mediated inflammation and CD8+ are T cell-mediated cytolysis; major triggers are autoimmunity, exaggerated or persistent responses to environmental Ags and some microbial Ags; tissue injury is caused by inflammation induced by cytokines, mainly Th1 and Th17 cells, macrophages, and/or killing of host cells by CD8+ CTLs

20
Q

What are the diseases of Type IV Hypersensitivity?

A
  • Multiple Sclerosis
  • Rheumatoid Arthritis
  • Type 1 (insulin-dependent) Diabetes Mellitus
  • Crohn’s Disease
  • Contact hypersensitivity (poison ivy reaction)
  • Chronic infections (tuberculosis)
21
Q

Describe Delayed-Type Hypersensitivity

A

Injurious cytokine-mediated inflammatory reaction resulting from activation of CD4+ T cells; develops 24-48 hrs after Ag exposure; may be sensitized for DTH reactions by microbial infection (TB) or by contact sensitization with poison ivy, metals, or some chemicals

***PPD (protein Ag of mycobacterium tuberculosis) elicits a DTH reaction, called the tuberculin reaction

22
Q

Explain Allergic Contact Dermatitis (ACD)

A

Caused by environmental exposure to external Ags that in contact with the skin trigger inflammatory reaction; results from a DTH reaction; metals are most common Ags

  • Sensitization to metals can occur at any age, even in neonates
  • Costume jewelry, particularly earrings, is linked to increased sensitization to nickel and cobalt
  • most common source of sensitization to chromium is leather