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Fundamentals of P > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

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

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?

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
Q

Describe naming of allergens

A

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
Q

Filaggrin and Atopic Dermatitis - describe relation to one another

A

Filaggrin links skin integrity and allergy
When it is defective atopic dermatitis is greater
This is due to the access for allergens

27
Q

What Makes Dendritic Cell Pro-Allergic?

A

Not Known
but
One Candidate Protein is TSLP
This may switch DC to a ‘pro-allergic’ state

(TSLP= Thymic stromal lymphopoietin)

28
Q

Describe mast cell activation

A

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
Q

Early and late phase allergic response - describe its mediators

A

Allergic responses have an early and late phase
Early is mediated by mast cells
Late is mediated by T cells

30
Q

Acute Allergic

Reaction - describe

A

Acute Allergic
Reaction

Wheezing
Urticaria
Sneezing,rhinorrhea
Conjunctivitis

31
Q

Chronic Allergic

Reaction - describe

A

Chronic Allergic
Reaction

Further wheezing
Sustained blockage
of the nose
Eczema

32
Q

Histamine - function

A

Effector mediator produced by mast cells:

increase vascular permeability
cause smooth muscle contraction

33
Q

Leukotrienes - function

A

Effector mediator produced by mast cells:

increase vascular permeability
cause smooth muscle contraction
stimulates mucus secretion

34
Q

Prostaglandins - function

A

Effector mediator produced by mast cells:

chemoattractants for T cells,
eosinophils and basophils

35
Q

Il-4 + IL-13 - function

A

Effector mediator produced by mast cells:

promotes Th2
promotes IgE

36
Q

TNF-α - function

A

Effector mediator produced by mast cells:

promotes tissue inflammation

37
Q

Mast cell activation - effect on GI tract

A

Increases fluid secretion + peristalsis

=

Expulsion of GI contents (diarrhea, vomiting)

38
Q

Mast cell activation - effect on airways

A

Decreased diameter, increased mucus secretion

=

Congestion/blockage (wheezing, coughing, phlegm)

Swelling/mucus secretion in nasal passages

39
Q

Mast cell activation - effect on BVs

A

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
Q

Eosinophils - location + why are they recruited

A

Eosinophils:
located in the tissues
recruited to the sites of allergic reactions
express FcεRI upon activation

41
Q

The two effector functions of eosinophils:

A

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
Q

The late phase of the IgE-mediated allergic response - characteristics

A

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
Q

The late phase of allergic response - explain the potentiation of further responses

A

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
Q

Explain how an allergy develops by comparing sensitisation/reaction

A

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
Q

Asthma - define

A

“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
Q

Non-atopic asthma includes what

A

Non Atopic includes:

Occupational
Exercise induced
Nocturnal Asthma
Post-bronchiolitic Wheeze

47
Q

Allergic Asthma - characteristics

A

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
Q

Allergic Asthma - describe acute response

A

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
Q

Allergic Asthma - describe chronic response

A

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
Q

Blockage of effector pathways: - describe

A

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
Q

How can you inhibit effects of mediators on specific receptors

A

inhibit effects of mediators on specific receptors

- anti-histamine (block the histamine H1 receptor)

52
Q

How can you inhibit mast cell degranulation

A

inhibit mast cell degranulation

mast cell stabilizer (e.g. chromoglycate)

53
Q

How can you inhibit synthesis of specific mediators

A 
inhibit synthesis of specific mediators
 lipoxygenase inhibitors (e.g montelukast)
54
Q

Describe use of steroids in allergies

A

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
Q

Describe use of bronchodilators in allergies

A

Bronchodilators – Reverse acute effect of allergy on airways (e.g B2 agonist salbutamol)

56
Q

Describe use of immunotherapy in allergies

A

Immunotherapy – Reverses the sensitisation to allergen by means of tolerising exposure

57
Q

Describe 2 important phases of allergies

A

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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