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Immuno-Sero LEC > HYPERSENSITIVITY > Flashcards

HYPERSENSITIVITY Flashcards

1
Q

• Normal but exaggerated or uncontrolled immune response to an antigen that can produce inflammation, cell destruction, or tissue injury

A

HYPERSENSITIVITY

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2
Q

antigen can persist, and the immune response can cause damage to the host

A

Hypersensitivity

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3
Q

Time of exposure

A

Immediate
Delayed

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4
Q

• Time of exposure
• Immediate-
Delayed-

A

antibody mediated
IgE, IgG, IgM

cell mediated
T-helper cells
48-72 hours

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5
Q

TYPES OF ANTIGENS AND REACTIONS

A

Latex allergies
Environmental substances
Infectious agents
Food allergies

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6
Q

Latex Allergies
• High-risk group:
- Latex:

A

children with frequent medical treatment or lengthy surgeries

natural rubber product

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7
Q

Reactions:
• IgE-mediated allergic reactions
• Cell-mediated contact dermatitis
• Irritant dermatitis

A

Latex

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8
Q

Environmental Substances

A

Allergens
Haptens
Toxin and irritants
Drug administration

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9
Q

• Influenza virus
• Damage epithelial cells in the respiratory tract
• Cytokine storm

A

Infectious Agents

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10
Q

• Cow’s milk, soy, chicken eggs, peanuts, tree nuts, wheat, fish, and crustaceans
• No current treatment available

A

Food Allergies

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11
Q

TYPE I HYPERSENSITIVITY
Aka

A

(Anaphylactic Hypersensitivity)

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12
Q

•______ derived from the Greek word atopos (meaning “out of place”): an inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens

A

Atopy

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13
Q

• passive cutaneous anaphylaxis

A

Carl Wilhelm Prausnitz and Heinz Küstner (1921):

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14
Q

• Triggered by allergens (peanuts, eggs, and pollen)
• Immediate allergic reactions

A

TYPE I HYPERSENSITIVITY
(Anaphylactic Hypersensitivity)

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15
Q

TYPE I HYPERSENSITIVITY
IMMUNOLOGIC MECHANISM
-

A

Sensitization Phase
Activation phase
Late phase

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16
Q
  • Sensitization Phase
  • First exposure leads to\____ production and mast cell sensitization.
    • Th2 cells release cytokines (3)
    • These cytokines prompt B cells to turn into plasma cells, which produce IgE antibodies specific to that allergen.
    • The IgE antibodies attach to mast cells and basophils, preparing them for future encounters with the allergen.
A

IgE

like IL-4, IL-5, and IL-13.

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17
Q

• Re-exposure triggers the immediate release of histamine and other mediators, causing rapid allergic symptoms.

A

Activation Phase

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18
Q

Inflammatory mediators:

A

histamine, heparin and tryptase

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19
Q
  • Chronic inflammation results from the recruitment of immune cells, leading to prolonged symptoms.
A
  • Late Phase
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20
Q

TYPE I HYPERSENSITIVITY
CLINICAL MANIFESTATIONS

A

Allergic rhinitis
Asthma
Urticaria
Angioedema
Anaphylaxis
Food allergies
Drug allergies
Eosinophilic esophagitis

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21
Q

: Sneezing, nasal congestion, and itchy eyes.

: Wheezing, shortness of breath, and coughing.

: Red, itchy, raised hives on the skin.

: Swelling of deeper tissues, especially in the face and throat.

A
  • Allergic Rhinitis
  • Asthma
  • Urticaria
  • Angioedema
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22
Q

: Severe, systemic reaction with rapid onset of symptoms, including difficulty breathing and hypotension.

: Oral, gastrointestinal, skin, and
respiratory symptoms after ingesting allergenic foods.

: Skin reactions, respiratory symptoms, and anaphylaxis.

: Swallowing difficulties and chest pain due to allergic inflammation in the esophagus.

A
  • Anaphylaxis

• Food Allergies

• Drug Allergies

  • Eosinophilic Esophagitis
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23
Q

TYPE I HYPERSENSITIVITY
TREATMENT

  • Pharmacological
A

• Antihistamines
- Corticosteroids
• Leukotriene Receptor Antagonist
• Beta-2-Adrenergic Agonists
• Mast cell stabilizers
• Epinephrine

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24
Q

TYPE I HYPERSENSITIVITY
TREATMENT

(Allergen-specific)

A

• Immunotherapy

25
Q

TYPE I HYPERSENSITIVITY
TREATMENT

• Emergency treatment of anaphylaxis

A

• Epinephrine
• Oxygen
• Intravenous fluids
• Antihistamine and corticosteroids

26
Q

TYPE I HYPERSENSITIVITY
DETECTION/TESTS

A

Skin testing
Serological tests
Challenge testing

Others
Nasal smear
Exhaled Nitric Oxide (FeNO)

27
Q
  • Skin testing (3)
  • Serological tests (2)
A
  • Skin Prick Test (SPT)
    • Intradermal test
  • Patch test

• Total Serum IgE
- Allergen-Specific (RAST)

28
Q

TYPE II HYPERSENSITIVITY
Aka

A

(Antibody-Mediated Cytotoxic Hypersensitivity)

29
Q

• Involves IgG and IgM antibodies directed against antigens found on cell surfaces.

• antigens may be altered self-antigens or heteroantigens

A

TYPE II HYPERSENSITIVITY
(Antibody-Mediated Cytotoxic Hypersensitivity)

30
Q

TYPE II HYPERSENSITIVITY
(Antibody-Mediated Cytotoxic Hypersensitivity)

• Binding of the antibody to a cell can have one of three major effects

A

• cell can be destroyed
• function of the cell can be inhibited
- function of the cell can be increased above normal

31
Q

TYPE II HYPERSENSITIVITY
MAJOR EFFECTS: Cell Damage

Cytotoxicity
Mechanism:

Examples:

A

• Complement activation
• Opsonization
- Antibody-Dependent Cellular Cytotoxicity (ADCC)

  • Blood Transfusion reactions
    • Hemolytic Disease of the Newborn (HDN)
    • Autoimmune Hemolytic Anemia
32
Q

TYPE II HYPERSENSITIVITY
MAJOR EFFECTS: Inhibition/Stimulation of Cell Function

• Dysfunction of the affected tissue or organ

• Enhance activity beyond normal levels

A

• Functional Impairment

• Overactivation

33
Q

TYPE II HYPERSENSITIVITY
MAJOR EFFECTS: Inhibition/Stimulation of Cell Function

• Autoantibody binds to ACH receptor= MUSCLE WEAKNESS

• TSI bind to TSH receptor on thyroid cells=excessive thyroid hormone production= HYPERTHYROIDISM

A
  • Myasthenia Gravis

• Grave’s Disease

34
Q

TYPE II HYPERSENSITIVITY
CLINICAL EXAMPLES
- Transfusion Reactions
• Mechanism

A
  • Mismatched blood transfusion
    • Antibody-Antigen binding
  • Complement activation
    • Hemolysis and tissue damage
35
Q

TYPE II HYPERSENSITIVITY
CLINICAL EXAMPLES

  • Clinical Manifestation
A

• Immediate Symptoms: Fever, chills, back pain, tachycardia, and hypotension
• Hemoglobinuria
• Jaundice

36
Q

TYPE II HYPERSENSITIVITY
CLINICAL EXAMPLES

• Mechanism
• Rh incompatibility
• Sensitization of the Mother
• Subsequent pregnancy
• Destruction of fetal RBCs

A

• Hemolytic Disease of the Newborn

37
Q
  • Clinical Manifestation
    • Anemia
  • Hydrops Fetalis
    • Jaundice
  • Enlarged Liver and Spleen
A

• Hemolytic Disease of the Newborn

38
Q

TYPE II HYPERSENSITIVITY
CLINICAL EXAMPLES

A
  • Autoimmune hemolytic Anemia (AIHA)
    • Goodpasture Syndrome
  • Grave’s Disease
    • Myasthenia Gravis
    • Pernicious Anemia
39
Q

TYPE II HYPERSENSITIVITY
DETECTION/TESTS

A

• Direct Antiglobulin Test (DAT) or
Direct Coombs Test

• Indirect Antiglobulin Tests (IAT) or Indirect Coombs Test

40
Q

TYPE II HYPERSENSITIVITY
DETECTION/TESTS

• Detects Abs/complement on the surface of RBCs

• Detects free Abs in the serum that can bind to RBC Ags

A

• Direct Antiglobulin Test (DAT) or
Direct Coombs Test

• Indirect Antiglobulin Tests (IAT) or Indirect Coombs Test

41
Q

TYPE II HYPERSENSITIVITY
DETECTION/TESTS

  • Measure specific autoantibodies

• Quantifies surface-bound antibodies on cells

• Detects Abs deposition in tissues

A

• Enzyme-Linked Immunosorbent Assay (ELISA)

• Flow Cytometry

• Tissue Biopsy with Immunofluorescence

42
Q

TYPE III HYPERSENSITIVITY
Aka

A

(Immune Complex-Mediated)

43
Q

Mechanism

• Immune complex formation
• Ag-Ab complex in circulation
• Immune complex deposition
• Blood vessel walls, kidneys, joints and lungs
- Activation of complement
• Release of C3a and C5a (inflammatory mediators)
- Inflammatory response
• Release lysosomal enzymes and reactive oxygen species
- Tissue injury
• Vasculitis, glomerulonephritis, arthritis

A

TYPE III HYPERSENSITIVITY
(Immune Complex-Mediated)

44
Q

TYPE III HYPERSENSITIVITY
CLINICAL EXAMPLES

• autoantibodies form against nuclear components
• Immune complexes deposit in kidneys, skin, joints and other organs

A
  • Systemic Lupus Erythematosus (SLE)
45
Q

TYPE III HYPERSENSITIVITY
CLINICAL EXAMPLES

• autoantibodies form immune complexes with IgG
• deposit in the synovial joints, leading to chronic inflammation and joint damage.

A

Rheumatoid Arthritis (RA)

46
Q

TYPE III HYPERSENSITIVITY
CLINICAL EXAMPLES

A

Serum sickness
Post-streptococcal Glomerulonephritis
Arthus reaction

47
Q

TYPE III HYPERSENSITIVITY
CLINICAL EXAMPLES

• foreign proteins are introduced into the body
• formation of immune complexes that deposit in blood vessels.

• formation of immune complexes
• deposit in the kidneys, leading to glomerular inflammation

  • Ag is injected into an individual with high levels of circulating Abs
    • Immune complexes form at the site of injection, leading to localized inflammation.
A

• Serum Sickness

• Post-Streptococcal Glomerulonephritis

  • Arthus Reaction
48
Q

TYPE III HYPERSENSITIVITY
DETECTION/TESTS

A

• Immune Complex Detection
• Complement Levels (C3, C4).
• Tissue Biopsy with Immunofluorescence
- ANA and Anti-dsDNA Tests.
• Rheumatoid Factor Test
• Cryoglobulin Test

49
Q

TYPE IV HYPERSENSITIVITY
Aka

A

(Delayed-Type Hypersensitivity)

50
Q

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)
- Described by_____
-______ to develop after antigen exposure
• driven by________

A

Robert Koch (1890)

48 to 72 hours

T cells and macrophages

51
Q

TYPE IV HYPERSENSITIVITY

Mechanisms:

A

• Sensitization Phase
- Effector Phase (Subsequent Exposure)
- Inflammation and Tissue Damage

52
Q

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)

1-2 weeks after the first contact with Ag
APCs process the Ag and present it to CD4+ helper (Th1) cells

  • Th1 cells become sensitized to the antigen and proliferate, generating a population of memory T cells that are specific to the antigen.
A

Sensitization Phase

53
Q

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)

• Upon re-exposure to the same antigen, these sensitized Th1 cells recognize the antigen and become activated.
• Activated Th1 cells==IFN-y
and TNF==macrophages to site of antigen exposure
• Macrophages==lysosomal enzymes, ROS, pro-inflammatory cytokines==tissue damage

A

Effector Phase (Subsequent Exposure)

54
Q

Inflammation and Tissue Damage

• The influx of immune cells
leads to inflammation and tissue damage at the site of antigen exposure, which manifests clinically as a delayed hypersensitivity reaction.

A

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)

55
Q

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)

• Development of granulomas that release large amounts of lytic enzymes that can destroy surrounding tissue and promote fibrin deposition

A

Chronic Type

56
Q

TYPE IV HYPERSENSITIVITY
(Delayed-Type Hypersensitivity)

Chronic Type
Triggers:
: M. tuberculosis, M. leprae, P. carinii, Leishmania spp and herpes simplex virus

: poison ivy, poison oa, metals, hair dyes and cosmetics

A

Intracellular

Contact Ag

57
Q

TYPE IV HYPERSENSITIVITY
CLINICAL EXAMPLES
• Contact Dermatitis
• Common Cause:_______
• poison ivy, poison oak, and poison sumac

• Signs:
• erythema, swelling, and the formation of papules that appears from 6 hours to several days after the exposure

• Duration:_____

A

URUSHIOL

3-4 weeks

58
Q

TYPE IV HYPERSENSITIVITY
CLINICAL EXAMPLES

• inflammation of the alveoli and interstitial spaces.

• Common Cause
- Bacterial and fungal spores

• Symptoms
• a dry cough, shortness of breath, fever, chills, weight loss, and general malaise

A

• Hypersensitivity Pneumonitis

59
Q

TYPE IV HYPERSENSITIVITY
DETECTION/TESTS

A
  • Patch Testing
    • Tuberculin Skin Test (Mantoux Test)
  • Candida and Other Skin
    Antigens
    • Granuloma Formation (via Biopsy)

Immuno-Sero LEC (25 decks)

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