Hypersensitivity Flashcards

1
Q

What 3 types of antigens can trigger hypersensitivity possibly leading to chronic diseases?

A
  1. Self-antigen
  2. Microbial antigen
  3. Environmental antigen
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2
Q

What is Type I Hypersensitivity also known as?

A

Immediate, IgE-mediated, allergy/atopy Hypersensitivity

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3
Q

Describe Type I Hypersensitivity

A
  1. Timing: within seconds to minutes
  2. Involves antigen-specific IgE on effector cells
  3. Vasoactive (Histamine) & eicosanoids and cytokines are released

*Most common type of hypersensitivity

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4
Q

Allergic rhinitis (hay fever), atopic asthma, anaphylaxis are examples of

A

Type I Hypersensitivity

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5
Q

Which types of Hypersensitivity are mediated by antibodies?

A

Type I, II, and III

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6
Q

Which type of hypersensitivity is local, tissue/cell specific?

A

Type II

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7
Q

Which type of hypersensitivity is general/systemic and related to immune complex deposition?

A

Type III

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8
Q

Which immunoglobulins have subtypes/subclasses?

A

IgA (2) & IgG (4)

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9
Q

Which immunoglobulin has the highest concentration and the longest half-life in the serum?

A

IgG

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10
Q

Which immunoglobulins have different forms?

A

IgA (monomer, dimer) & IgM (monomer, pentamer)

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11
Q

What is Type II Hypersensitivity also known as?

A

Antibody-mediated, cytotoxic

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12
Q

Describe Type II Hypersensitivity

A
  1. Timing: within minutes to hours
  2. Involves IgM and IgG
  3. 3 mechanisms
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13
Q

What is the complement and Fc receptor mediated mechanism of Type II Hypersensitivity?

A

Antibodies bind to antigens (allow direct binding of phagocytes on Fc portion) or activate complement (through classical pathway) which leads to inflammation (attract neutrophils).

Ex. Goodpasture Syndrome

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14
Q

Describe Goodpasture Syndrome

A

aka. anti-glomerular basement membrane disease

Antibodies are produced against basement membrane in kidney and lung.

Symptoms: bloody urine/lung, kidney failure

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15
Q

What is the opsonization and phagocytosis mechanism of Type II Hypersensitivity?

A

Antibodies opsonize the outside of cells and then phagocytes come and eat them up.

Ex. Idiopathic Thrombocytopenic Purpura (No platelets)
Ex. Autoimmune Hemolytic Anemia (AIHA)

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16
Q

Describe ITP

A

Auto-antibodies are produced against platelets. Platelets are opsonized and removed in the spleen.

Symptoms: easy/persistent nose bleeding

17
Q

Describe AIHA

A

Auto-antibodies are produced against RBC membrane proteins.

Symptoms: faigue, jaundice, pallor (pale skin), weakness

18
Q

What is the abnormal physiologic responses without cell/tissue injury mechanism of Type II Hypersensitivity?

A
  1. Graves’ Disease: Antibody binds TSH receptor (turns it on) without the presence of hormone/ligand. Causes hyperthyroidism.
  2. Myasthenia Gravis: Antibody binds ACh receptor and prevents ACh hormone from binding and signaling muscle contraction.
19
Q

Acute rheumatic fever (myocardial antigens), pemphigus vulgaris (desmosomes), and pernicious anemia (intrinsic factors) are examples of

A

Type II Hypersensitivity

20
Q

What is Type III Hypersensitivity also known as?

A

Immune Complex mediated

21
Q

Describe Type III Hypersensitivity

A
  1. Timing: within hours
  2. Involves IgM and IgG
  3. Due to accumulations of immune complexes in vessels, joints causing complement/Fc receptor inflammation leading to attraction of neutrophils/macrophages (vasculitis).

Ex. Serum Sickness
Ex. Systemic Lupus Erythematosus (SLE)

22
Q

What is an immune complex?

A

an antigen-antibody complex

23
Q

What is serum sickness?

A

A phenomenon when patient makes antibodies against the foreign horse antibodies (against diphtheria) causing complex formation and deposition.

24
Q

Describe SLE

A

SLE has type II hypersensitivity with blood (low WBC, RBC, and platelets), but majority of lupus symptoms are classic type III.

Symptoms: Malar rash (butterfly), fever, joint pain

25
Q

Poststreptococcal glomerulonephritis (group A strep antigen) and polyarteritis nodosa (HBV surface antigen) are examples of

A

Type III hypersensitivity

26
Q

What is Type IV Hypersensitivity also known as?

A

Delayed Type, cell-mediate

27
Q

Describe Type III Hypersensitivity

A
  1. Timing: Days (slowest)
  2. Involves T cells (CD4 or CD8)–> 2 mechanisms
  3. Not transferrable by serum like in case of antibodies
28
Q

What is cytokine-mediated inflammation mechanism of Type IV Hypersensitivity?

A

APC presenting tissue antigen is recognized and bound by CD4 T cell. IFN-y is released and causes inflammation (attraction of macrophages, neutrophils) and tissue injury.

Ex. TST

29
Q

What is another name for TST or PPD test for tuberculosis?

A

Mantoux Test

30
Q

What is T cell mediated killing of host cells mechanism of Type IV Hypersensitivity?

A

Host cell infected with antigen presents MHC I + peptide and is recognized by CD8 for direct killing leading to cell death/tissue injury.

Ex. Contact Dermatitis (poison ivy)

31
Q

Describe Poison Ivy contact dermatitis

A

The antigen, urushiol (colorless oil) is lipid soluble so crosses cell membrane and gets presented by cells (MHC I). CTL recognizes, binds, and triggers cell destruction/apoptosis.