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Fundamentals of P > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

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1
Q

Types of hypersensitivity

A

Type 1: immediate hypersensitivity

Type 2: cytotoxic hypersensitivity

Type 3: serum sickness and Arthus reaction

Type 4: delayed-type hypersensitivity, contact dermatitis

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2
Q

Hypersensitivity - define

A

An inappropriate immune response to non-infectious antigens that results in tissue damage and disease

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3
Q

Systemic anaphylaxis - define

A

Systemic anaphylaxis is a life-threatening allergic event resulting in massive, generalized mast cell degranulation.

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4
Q

Type II hypersensitivity reactions respond to

A

Type II hypersensitivity reactions respond to altered components of human cells

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5
Q

Antibody-bound cells are cleared by:

A

Antibody-bound cells are cleared by:
FcγR+ cells such as macrophages

complement

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6
Q

Special case of a Type II response:

A

Special case of a Type II response:
involves IgG antibodies directed at cell-surface receptors
these antibodies disrupt the normal functions of the receptor by either:
uncontrollable activation or blocking receptor function

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7
Q

Examples of Type 2 HS

A

Grave’s disease
Myasthenia gravis
Hemolytic disease of the newborn

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8
Q

Myasthenia gravis - define

A

Antibodies block or destroy nicotinic acetylcholine receptors at the junction between the nerve and muscle

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9
Q

Grave’s disease - define

A

Graves’ disease is an autoimmune disorder that causes hyperthyroidism, or overactive thyroid.

Immune system attacks the thyroid = more TH made than needed

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10
Q

Hemolytic disease of the newborn - defomne

A

A blood problem in newborn babies. It occurs when your baby’s red blood cells break down at a fast rate

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11
Q

Type III - describe effector mechanism

A

IgG and soluble antigen form immune complexes

Immune complexes are cleared by phagocytes.

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12
Q

Describe events leading to occlusion of small BVs

A

activate mast cells to release inflammatory mediators.

inflammatory cells invade the site, and blood vessel permeability and blood flow are increased.

Platelets also accumulate, leading to occlusion of the small blood vessels, hemorrhage, and the appearance of purpura.

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13
Q

Serum sickness - cause

A

caused by large intravenous doses of soluble antigens (e.g. drugs)

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14
Q

Serum sickness - explain the tissue damage

A

IgG antibodies produced form small immune complexes with the antigen in excess.
immune complexes deposited in tissues e.g. blood vessel walls.
tissue damage is caused by complement activation and the subsequent inflammatory responses

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15
Q

What determines the pathology observed in type III hypersensitivity reactions

A

Antigen dose and route of delivery determine the pathology observed in type III hypersensitivity reactions

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16
Q

Time course of delayed (Type IV) hypersensitivity - describe

A

Antigen injected into subcutaneous tissue and processed by local antigen-presenting cells

A TH1 effector cell recognizes antigen and releases cytokines that act on vascular endothelium

Recruitment of phagocytes and plasma to site of antigen injection causes visible lesion

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17
Q

Mantoux test - desribe

A

The Mantoux test is a widely used test for latent TB.

It involves injecting a small amount of a substance called PPD tuberculin into the skin of your forearm. It’s also called the tuberculin skin test (TST).

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18
Q

Tuberculoid leprosy - describe

A

Type 4

Tuberculoid leprosy is a form of leprosy characterized by solitary skin lesions that are asymmetrically distributed with few lesions and well demarcated edges. There is also early and marked nerve damage.

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19
Q

Contact dermatitis - describe

A

Type 4

Contact dermatitis is a red, itchy rash caused by direct contact with a substance or an allergic reaction to it.

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20
Q

Poison ivy - describe

A

Poison ivy rash is a type of allergic contact dermatitis caused by an oily resin called urushiol.

This resin is very sticky, so it easily attaches to your skin, clothing, tools, equipment and pet’s fur.

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21
Q

Type I : Allergy - define

A 
defined as “disease
	following a response
	by the immune system
	to an otherwise 
	innocuous antigen”
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22
Q

What is IgE?

A

First line of defence against worms
Binds FcεR1 receptor on mast cells
Pre-arms mast cells to react when in the presence of antigen

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23
Q

Allergen-specific IgE Production:

The simple Model = describe

Study These Flashcards
A

First exposure to pollen

IL-4 drives B cells to produce IgE in response to pollen antigens
Pollen-specific IgE binds to mast cell

Second exposure to pollen

=

acute release of mast-cell contents causes allergic rhinitis (hay fever)

24
Q

What causes Allergic Sensitisation?

Study These Flashcards
A

What causes Allergic Sensitisation?

Exposure to Allergen is critical, this includes:
Nature of the allergen
Dosage of Allergen (high vs. low)
Timing
Location of Priming

Role of pro-allergic dendritic cells and cytokines

Genetic predisposition to Allergy

25
Describe naming of allergens
Allergens are named systematically: After the source organism and the order they were discovered e.g. Der p1 comes from Dermatophagoides pteronyssinus Not all proteins are allergenic
26
Filaggrin and Atopic Dermatitis - describe relation to one another
Filaggrin links skin integrity and allergy When it is defective atopic dermatitis is greater This is due to the access for allergens
27
What Makes Dendritic Cell Pro-Allergic?
Not Known but One Candidate Protein is TSLP This may switch DC to a ‘pro-allergic’ state (TSLP= Thymic stromal lymphopoietin)
28
Describe mast cell activation
Resting mast cell contains granules containing histamine and other inflammatory mediators Bound IgE is allergen-specific Specific allergen crosslinks IgE = Multivalent antigen cross-links bound IgE antibody, causing release of granule contents
29
Early and late phase allergic response - describe its mediators
Allergic responses have an early and late phase Early is mediated by mast cells Late is mediated by T cells
30
Acute Allergic | Reaction - describe
Acute Allergic Reaction Wheezing Urticaria Sneezing,rhinorrhea Conjunctivitis
31
Chronic Allergic | Reaction - describe
Chronic Allergic Reaction Further wheezing Sustained blockage of the nose Eczema
32
Histamine - function
Effector mediator produced by mast cells: increase vascular permeability cause smooth muscle contraction
33
Leukotrienes - function
Effector mediator produced by mast cells: increase vascular permeability cause smooth muscle contraction stimulates mucus secretion
34
Prostaglandins - function
Effector mediator produced by mast cells: chemoattractants for T cells, eosinophils and basophils
35
Il-4 + IL-13 - function
Effector mediator produced by mast cells: promotes Th2 promotes IgE
36
TNF-α - function
Effector mediator produced by mast cells: promotes tissue inflammation
37
Mast cell activation - effect on GI tract
Increases fluid secretion + peristalsis = Expulsion of GI contents (diarrhea, vomiting)
38
Mast cell activation - effect on airways
Decreased diameter, increased mucus secretion = Congestion/blockage (wheezing, coughing, phlegm) Swelling/mucus secretion in nasal passages
39
Mast cell activation - effect on BVs
Increased BF, increased permeability = Increased fluid in tissues = increased flow of lymph to lymph nodes Increased cells/protein in tissues Increased effector response in tissues
40
Eosinophils - location + why are they recruited
Eosinophils: located in the tissues recruited to the sites of allergic reactions express FcεRI upon activation
41
The two effector functions of eosinophils:
The two effector functions of eosinophils: 1. Release highly toxic granule proteins and free radicals upon activation to kill microorganisms/parasites and cause tissue damage in allergic reactions. 2. Synthesise and release prostaglandins, leukotrienes and cytokines in order to amplify the inflammatory response by activating epithelial cells and recruiting leukocytes.
42
The late phase of the IgE-mediated allergic response - characteristics
Late-phase reaction is dependent on allergen dose Continued synthesis and release of inflammatory mediators Chronic allergic inflammation caused by Th2 cells i.e. a type IV hypersensitivity reaction
43
The late phase of allergic response - explain the potentiation of further responses
The late phase of allergic response is T cell mediated: Mostly consisting of allergen specific Th2 cells These cells recruit other cells by cytokine release Potentiate further responses
44
Explain how an allergy develops by comparing sensitisation/reaction
There is a key difference between sensitisation to allergen and reaction to allergen. Individuals must be sensitised to an allergen before they can react. Sensitisation requires presentation of allergen to T cells by DC and the priming of Cognate B cells to produce IgE The Reaction to allergen occurs when the individual is re-exposed to allergen and it binds preformed IgE on mast cells
45
Asthma - define
“A State of reversible bronchial hyper-reactivity resulting from a persistent inflammatory process in response to a number of stimuli in a genetically susceptible individual”.
46
Non-atopic asthma includes what
Non Atopic includes: Occupational Exercise induced Nocturnal Asthma Post-bronchiolitic Wheeze
47
Allergic Asthma - characteristics
Characteristics: ``` episodes of wheezy breathing narrowing of the airways rapid changes in airway obstruction severity varies - slight wheeziness to asthma attack common allergens causing asthma include pollen HDM plants some foods ```
48
Allergic Asthma - describe acute response
Acute response: occurs within seconds of allergen exposure results in airway obstruction and breathing difficulties caused by allergen-induced mast cell degranulation in the submucosa of the airways
49
Allergic Asthma - describe chronic response
Chronic response: chronic inflammation of the airways caused by activation of eosinophils, neutrophils, T cells and other leukocytes ``` mediators released by these cells cause airway remodelling, permanent narrowing of the airways, and further tissue damage ```
50
Blockage of effector pathways: - describe
Blockage of effector pathways: inhibit effects of mediators on specific receptors anti-histamine (block the histamine H1 receptor) inhibit mast cell degranulation mast cell stabilizer (e.g. chromoglycate) ``` inhibit synthesis of specific mediators lipoxygenase inhibitors (e.g montelukast) ```
51
How can you inhibit effects of mediators on specific receptors
inhibit effects of mediators on specific receptors | - anti-histamine (block the histamine H1 receptor)
52
How can you inhibit mast cell degranulation
inhibit mast cell degranulation | mast cell stabilizer (e.g. chromoglycate)
53
How can you inhibit synthesis of specific mediators
``` inhibit synthesis of specific mediators lipoxygenase inhibitors (e.g montelukast) ```
54
Describe use of steroids in allergies
Steroids – Act directly on DNA to increase transcription of anti-inflammatory mediators (e.g. IL-10) and decrease transcription of pro-inflammatory mediators (e.g prednisolone)
55
Describe use of bronchodilators in allergies
Bronchodilators – Reverse acute effect of allergy on airways (e.g B2 agonist salbutamol)
56
Describe use of immunotherapy in allergies
Immunotherapy – Reverses the sensitisation to allergen by means of tolerising exposure
57
Describe 2 important phases of allergies
2 important phases: Sensitisation – allergen presented by DC to Th2 CD4 T cells and B cells Reaction – IgE on mast cells cross-linked by cognate antigen leading to inflammation

Fundamentals of P (62 decks)

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