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General Pathology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is an immune response?

A

The body’s response against antigens through the activation of its immune system

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2
Q

When does an immune response fail?

A

Too much: Hypersensitivity –> immunologic injury
Too little: Immunodeficiency
Wrong targets: Autoimmunity

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3
Q

What are the 2 arms of the immune response?

A
  1. Humoral (antibody) mediated - B lymphocytes, Plasma Cells
  2. Cell mediated - Macrophages, CD4 (effector/helper) and CD8 (cytotoxic) T-Lymphocytes
    * Antibody Independent!
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4
Q

What are the antibody effector functions>

A
  1. Neutralisation of Microbes and Toxins
  2. Opsonisation and phagocytosis
  3. Antibody dependent cytotoxicity (involves NK cells)
  4. Complement Activation
    a. Lysis of Microbes
    b. Phagocytosis of opsonised microbes
    c. Inflammation
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5
Q

Process of cell mediated immunity

A
  1. Dendritic cell with the antigen goes to the lymph node
  2. Naive T cells form Effector T Cells (CD4+) and Memory T Cells (CD8+)
  3. Differentiated T cells enter circulation
  4. Effector T cells (CD4+) migrate to site of antigen
  5. Cytokine secretion causing macrophage activation (killing of ingested microbes) and inflammation

meanwhile

  1. Memory T cells (CD8+) remain in circulation till it comes across an infected cell with microbes in cytoplasm
  2. Kills infected cells (Cytotoxic T Cell)
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6
Q

What is the difference between IgE and IgG?

A

IgE is an indication of a hypersensitivity or true allergy. IgG is a secondary response usually associated with a previous exposure to an antigen.

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7
Q

What is the difference between IgG and IgM?

A

IgG can take time to form after an infection or immunisation. IgM is found mainly in blood and lymph fluid and is the first antibody the body makes when it fights a new infection.

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8
Q

Which arm of the immune system are the hypersensitivity reactions caused by?

A

Hypersensitivity type I, II, III: Humoral (antibody) mediated - B Cells
Hypersensitivity IV: Cell mediated - T Cells

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9
Q

What is the duration of hypersensitivity reactions?

A

Hypersensitivity type I, II, III: Immediate (minutes to days)
Hypersensitivity IV: Delayed (few days to weeks, even months or years)

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10
Q

What are the types of hypersensitivity reactions?

A

Type I: Anaphylactic - Antibody (IgE) with mast cell
Type II: Cytotoxic - Antibody (non-IgE) with antigenic surface
Type III: Complex Mediated - Antigen + Antibody
Type IV: Cell Mediated (NO ANTIBODIES) - Antigens killed by NK cells and lymphokines

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11
Q

What is a type I hypersensitivity reaction?

A

Anaphylactic
Combination of an antigen with an antibody bound to mast cells or basophils in individuals previously sensitised.
Can be localised or systemic or both.

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12
Q

How long is the effect of a type I hypersensitivity reaction?

A

The effect is rapid (minutes) to sustained (hours to 1 to 2 days)

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13
Q

What is an example of a type I hypersensitivity reaction?

A

Hay Fever

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14
Q

What is the reaction process of a type I hypersensitivity reaction?

A

First Exposure

  1. Antigen presentation results in sensitisation - Antigen presenting cell activates the t-cell receptors on the t-helper cd4+ cells causing release of IL-4 and IL-5 + antigen activates IgE B cell
  2. IgE production by B cells
  3. Mast cells are armed with IgE antibodies on the IgE Fc receptors

Second Exposure

  1. Antigen cross links with the IgE antibodies on the mast cells leading to degranulation (release of primary and secondary mediators/chemokines)
  2. Clinical Effects
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15
Q

What are the factors that causes antigens to synthesise IgE antibodies?

A
  1. Type of antigen
  2. Route of antigen administration (mucosal penetration)
  3. Genetic factors (atopy implies familial predisposition to allergy)
  4. Environmental factors
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16
Q

What are the degranulation contents in mast cells?

A

Histamine

Proteases

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17
Q

What are the immediate hypersensitivity I reaction responses?

A
  1. Vasodilation (decrease BP)
  2. Vascular leakage -> local swelling
  3. Smooth muscle spasm/constriction
  4. Stimulation of mucus secretion
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18
Q

What are the immediate hypersensitivity I reaction responses caused by?

A
  1. Degranulation contents
  2. Membrane phospholipids -> arachidonic acid -> leukotrienes + prostaglandin
  3. Platelets activating factor
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19
Q

What are the late phase hypersensitivity I reaction responses?

A
  1. Leukocyte infiltration
  2. Epithelial damage
  3. Bronchospasm
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20
Q

What are the late phase hypersensitivity I reaction responses caused by?

A

Mediated by cytokines and chemokines
Mast cells: tryptase + chymase
Eosinophils: Proteolytic enzymes + eosinophil cationic protein

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21
Q

What medical condition is caused by type I hypersensitivity reactions?

A

Systemic Anaphylaxis leading to
1. Vascular Shock
Due to generalised vasodilation and vascular leak (esp in face and larynx)
2. Difficulty breathing
Bronchoconstriction (smooth muscle effect)
3. Widespread oedema

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22
Q

Why is systemic anaphylaxis life threatening?

A
  • Circulatory Failure

- Airway obstruction (laryngeal oedema + bronchoconstriction)

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23
Q

How does adrenaline/epinephrine help to counteract the effects of systemic anaphylaxis?

A
  1. Vasoconstriction of blood vessels
  2. Relaxes smooth muscles (in lungs to improve breathing)
  3. Improves cardiac output (stimulate heartbeat) - increase BP and O2 delivery to tissues
  4. Stop swelling around the face and lips (angioedema)
24
Q

What are local medical conditions caused by type I hypersensitivity reactions

A 
Skin: Urticaria, Pruritis and Angioedema
Eye: Watery Eye, Conjunctivitis
Bronchial Asthma
Allergic Rhinitis
Food Allergies: Increased Peristalsis
25
Q

What are the microscopic features of bronchial asthma?

A
  1. Excessive mucous secretion
  2. Submucosal inflammatory infiltrate with lymphocytes and eosinophils
  3. Thickened basement membrane
  4. Smooth muscle cell hyperplasia
26
Q

What is allergic rhinitis?

A

Allergic rhinitis occurs when your immune system reacts to particles (allergens) in the air that you breathe by causing an allergic reaction such as sneezing, inflammation and a runny nose.

27
Q

What are the types of allergic rhinitis?

A

Seasonal: seasonal pollens and outdoor moulds
Perennial: allergens within the home eg. house dust mites, pets, cockroaches, rodents
Sporadic: intermittent exposure to an allergen (all kinds)
Occupational: exposure to allergens in the workplace (can be a any of the 3 above)

28
Q

How do you diagnose hypersensitivity I reactions?

A

Skin patch test/Prick test - test for particular antigen

Blood test - detect certain antibodies (igG) in the blood

29
Q

What are the treatment options for hypersensitivity I reactions?

A
  1. Avoid the allergen (BEST)
  2. Antihistamines - neutralises histamines
  3. Corticosteroids Nasal Sprays - reduces inflammation causing swelling, sneezing and running nose
  4. Decongestants
  5. Allergy shots - immunotherapy by exposing the body to increasingly higher doses of the allergen
30
Q

What is type II hypersensitivity reactions?

A

Cytotoxic
Antibody (non-IgE) is directed against antigens on the cell membrane or in the extracellular matrix (antigenic surface, cell or basement membrane).
This binding is done by Fab segments (cytotoxic binding)
The carpet of fixed antibody fixes leukocytes and activates complements, thereby attracting even more leukocytes.
Damage to the antigenic surface is done by complement and by leukocytes.

31
Q

What is the difference between our bodies defense mechanism and cytotoxic type II hypersensitivity?

A

This binding initiates a defence mechanism when the target is a microbe or cancer cell
BUT
if it is binding to a surface (cytotoxic type II hypersensitivity) it causes disease when the surface marked for destruction is a normal part of the body.
It causes damage to the surface.

32
Q

What 3 routes can hypersensitivity II reactions be caused by?

A
  1. Phagocytosis (opsonisation via antibody)
  2. Inflammation - due to complement-medated reactions involving leukocytes)
  3. Cellular dysfunction - antibodies directed against cell surface receptors impair or dysregulate without causing cell injury of inflammation)
33
Q

What is the examples of type II hypersensitivity caused by phagocytosis?

A

Eg. Immune Haemolysis (autoimmune haemolytic anaemias, autoimmune thrombocytopenia) - platelets and RBCs are opsonised and phagocytosed

34
Q

What is the examples of type II hypersensitivity caused by inflammation (complement mediated)?

A
  1. Targeting of allograft in transplant rejection
  2. Goodpasture syndrome
  3. Pemphigus Vulgaris
  4. Isoimmune reactions to blood-group antigens - Transfusion reactions (ABO mismatch) or Maternofoetal incompatibility (Rh mismatch)
35
Q

What is the foreign surface in ABO mismatch?

A

Injected mismatched RBCs

They are attacked by the recipients antibodies causing agglutination and lysis

36
Q

What blood group is the universal donor?

A

Blood group O

37
Q

What blood group is the universal recipient?

A

Blood group AB

38
Q

What is the examples of type II hypersensitivity caused by cellular dysfuntion?

A
  1. Myasthenia Gravis - antibodies inhibit binding of neurotransmitter ACh to receptor causing muscular weakness
  2. Graves Disease - antibodies bind to TSH receptors, causing TH hormone to be stimulate without TSH
39
Q

What is the difference between Type III hypersensitivity reactions and Type II hypersensitivity reactions?

A

Type III: occurs in blood vessels; damage done by neutrophils
Type II: occurs on cell surface membrane/extracellular space; damage done by leukocytes and complements

40
Q

What are type III hypersensitivity reactions?

A

Cytotoxic
Antibody (non-IgE) is directed against antigens found within the blood vessel
This binding is done by Fab segments (cytotoxic binding)
Complexes fix leukocytes and activates complements, thereby attracting even more leukocytes.
Damage to the antigenic surface is done mainly by neutrophils

41
Q

What are in situ immune complexes?

A

Binding reaction of antigen to antibody occurs within circulation then gets excreted out to extravascular sites of deposition. (Still Type III not Type II hypersensitivity because it begins within the blood vessel)

42
Q

What are circulating immune complexes?

A

Binding reaction of antigen to antibody occurs within the circulation

43
Q

Are complexes being produced in circulation always pathogenic?

A

No, only if they are produced in large amounts, persist and are deposited in tissues

44
Q

What are the phases of type III hypersensitivity?

A

Phase 1: Formation of antigen-antibody complexes in the circulation
Phase 2: Deposition of immune complexes in various tissues (eg. glomeruli, myocardium, joints)
Phase 3: initiation of an inflammatory reaction in dispersed sites throughout the body
a. Activation of complement cascade
b. Activation of neutrophils + macrophages)

45
Q

What is fibrinoid necrosis?

A

Damage in blood vessels caused by deposition of immune complexes, causing vasculitis/small vessel disease

46
Q

What are damages caused by type III hypersensitivity?

A
  1. Vasculitis (vessels)
  2. Glomerulonephritis (Glomeruli)
  3. Arthritis (Joint synovium)
47
Q

What is an example of a disease caused by Type III hypersensitivity?

A 
Lupus Erythematosus
Symptoms (all manifestations of vascular damage):
Butterfly rash
Pleural Effusions
Heart problems
Lupus Nephritis
Arthritis
Raynaud's phenomenon
48
Q

What is special about Type IV hypersensitivity reactions?

A

It is cell-mediated hence there is no antibody involvement.

Instead, target antigenic cells are killed by killer cells and lymphokines

49
Q

What is Type IV hypersensitivity reactions?

A

A type of chronic inflammation initiated by specifically sensitised T-lymphocytes:
CD4 T-cells: delayed-type hypersensitivity (cytokine mediated inflammation, phagocytes, macrophages)
CD8 T-cells: direct cell cytotoxicity

50
Q

What is Granulomatous Inflammation?

A

Immune Granulomas are caused by particles that elicit a cell-mediated immune response (T-lymphocytic response) in the context of cytokines (IL-2 and IFN-y)

51
Q

What is the difference between a foreign body granuloma, and an immune granuloma?

A

Foreign body granulomas do not involve T cells while immune granulomas are caused by immune cells

52
Q

What is special about how CD8+ cytotoxic T lymphocytes kill target antigen cells in type IV hypersensitivity?

A

They also secrete cytokines IFN-y that are involved in inflammatory reactions similar to delayed type hypersensitivity

53
Q

In dental surgery, what are the 2 types of hypersensitivity reactions that occur?

A

Type I hypersensitivity (IgE)- Allergen
Type IV hypersensitivity (T-lymphocytes) - contact sensitivity caused by various environmental chemicals eg. amalgam/local anaesthetic

All types of drugs, dental materials and toothpastes/mouth rinses can cause hypersensitivity reactions
Gloves can also cause hypersensitivity reactions in dental personnel

54
Q

What type of hypersensitivity reaction is transplant rejection caused by?

A

it involves different hypersensitivity reactions (complex reaction) which occurs if there is a lack of compatibility of the HLA system between donor and host
Eg. Type II + IV delayed + IV cytotoxic

55
Q

What is an example of a delayed type IV hypersensitivity reaction in dentistry?

A

Lichenoid Oral Lesions - whitish lacelike patch appearance, sometimes with ulcers within, found on mucosa of cheeks
Caused by hyperkeratosis and consists of a lot of T-cells)

56
Q

What is contact allergy?

A

A type IV hypersensitivity caused by direct contact with allergen
Eg.
Desquamative gingivitis - gingival tissues demonstrate potentially painful erythema, haemorrhage, sloughing, erosion and ulceration
Stomatitis - redness and swelling that may occur in any part of the mouth

Patch testing is used to identify the specific antigen (biopsy used as histological evidence to support the diagnosis)

General Pathology (10 decks)

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