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Immunity > Session 1 - Hypersensitivity Reactions > Flashcards

Session 1 - Hypersensitivity Reactions Flashcards

1
Q

What is the main role of the adaptive and innate immune system?

A

Protection and prevention against infection = success

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2
Q

What can lead to failure of the immune system?

A
  • non-self, Infection, altered self (e.g. cancer)
  • immunodeficiency (primary and secondary Disorders)
  • autoimmune disease
  • allergies
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3
Q

Give the definition of hypersensitivity.

A

The antigen (or antigen driven) specific immune responses that are either inappropriate or excessive, and result in harm to host.

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4
Q

What are the 2 types of antigenic triggers?

A

Hypersensitivity to exogenous antigensm

  • non infectious substances (innocuous)
  • infectious microbes
  • Drugs (penicillin)

Hypersensitivity to intrinsic antigens:

  • infectious microbes (mimicry)
  • self antigens (autoimmunity)
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5
Q

What are the different types of hypersensitivity reactions?

A

Type I = immediate (allergy) = environmental non infectious antigens. IgE mediated.
Type II = antibody mediated = against cell bound antigen (on tissue). IgG/IgM mediated.
Type III = immune complex mediated = against soluble antigen (can deposit). IgG/IgM mediated.
Type IV = Cell mediated (delayed) = environmental infectious agents and self antigens.

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6
Q

What are the common features of hypersensitivity reactions?

A
  • sensitisation phase

- effector phase

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7
Q

What is the sensitisation phase?

A

First encounter with the antigen. Activation of APCs and memory effector cells. A previously exposed individual to the antigen is said to be sensitised. No clinical manifestation = no signs/symptoms

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8
Q

What is the effector phase?

A

Pathological reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity. Get clinical manifestation = signs/symptoms.

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9
Q

Give the characteristics of a type II hypersensitivity reaction.

A
  • usually develops within 5 - 12 hrs
  • involves IgG or IgM antibodies
  • targets cell bound antigens = exogenous (blood Group antigens, rhesus D antigens), endogenous (self antigens)
  • induces different outcomes = tissue/cell damage or physiological change (change in organ function = bad)
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10
Q

What are the mechanisms of type 2 hypersensitivity reactions in relation to tissue/cell damage?

A

1) complement activation:
- Cell lysis (macrophages)
- neutrophil recruitment/activation (C3a/C5a)
- Opsonisation (C3b)
- e.g. haemolytic Disease Of The newborn (Rheus D antigen), transfusion reactions (ABO)

2) Antibody dependent cell cytotoxicity = natural killer cells
- e.g. autoimmune haemolytic Anaemia (warm and cold), immune thrombocytopenia purpura (lose platelets), goodpastures syndrome

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11
Q

Why is complement pathway important in type II hypersensitivity reactions?

A

Complement regulate innate and adaptive immune system.

Also clears immune complexes

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12
Q

Explain the process by which haemolytic disease if the newborn occurs.

A

1) Rh+ father
2) Rh- mother carrying her first Rh+ foetus. Rh antigens from the developing foetus can Exeter the mother’s blood during delivery.
3) in response to the foetal Rh antigens the mother will produce anti-Rh antibodies.
4) if the woman becomes pregnant with another Rh+ foetus, her anti-Rh antibodies will cross the placenta and damage foetal red blood cells.

Immunoglobulin against Rh factor given within 72hrs of delivery.

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13
Q

What are the mechanisms of Type II hypersensitivity reactions in relation to physiological change?

A

1) Receptor stimulation
- e.g. Graves’ disease = increased thyroid activity (antigen = TSH receptor)

2) receptor blockade
- e.g. Myasthenia gravis = impaired neuromuscular signalling (antigen = acetylcholine receptor)

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14
Q

What are the therapeutic approaches to type II hypersensitivity reactions?

A

Tissue/cell damage:

  • anti inflammatory drugs = complement activation
  • plasmapheresis = circulatory antibodies and inflammatory mediators
  • splenectomy = opsonisation/phagocytosis
  • intravenous immunoglobulin (IVIG) = IgG degradation

Physiological change:

  • correct metabolism = antithyroid Drugs In Graves’ disease
  • replacement therapy = Pyridostigimine (inhibits ACh esterase) in MG
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15
Q

What type II hypersensitivity Conditions would plasmapheresis be used for?

A

Myasthenia gravis
Goodpastures syndrome
Graves’ disease

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16
Q

Name some characteristics of type III hypersensitivity reactions.

A
  • usually develops within 3-8 hrs
  • involves immune complexes between IgG or IgM antigens
  • targets soluble antigens = foreign (Infection) and endogenous (self antigens)
  • tissue damage caused by the deposition of immune complexes in host tissues
17
Q

What are the key factors affecting IC pathogens is in type III hypersensitivity reactions?

A

1) complex size:
- small and large ICs cleared
- intermediate size ICs
2) host response:
- low affinity antibody
- complement deficiency
3) local tissue factors:
- haemodynamic factors
- physio chemical factors

18
Q

What can persistence of ICs in type III hypersensitivity reactions lead to?

A

Deposition = joint, kidney, small vessels, skin

Multisystem disease

19
Q

What is the mechanism of type III hypersensitivity reactions?

A

1) intermediate sized immune complexes deposited in the tissue
2) complement activated
3) neutrophil chemotaxis
4) neutrophil adherence and degranulation

20
Q

Give some examples of diseases caused by type III hypersensitivity reactions.

A

1) rheumatoid arthritis = immune complex deposition in areas of high blood flow e.g. kidney, knee, liver
2) glomerulonephritis (infectious) = bacterial endocarditis, hepatitis B infection
3) systemic lupus erythematous

21
Q

Name some of the characteristics of type IV hypersensitivity reactions.

A
  • usually develops within 24-72 hrs
  • involves lymphocytes and macrophages
  • different subtypes (clinical outcomes) = contact hypersensitivity, tuberculin hypersensitivity, granulomatous hypersensitivity
22
Q

Give some examples of diseases caused by type IV hypersensitivity reactions to exogenous antigens.

A

Contact hypersensitivity:

  • epidermal reaction
  • require endogenous proteins
  • e.g. nickel, poison ivy, organic chemicals

2) granulomatous hypersensitivity:
- 21 - 48 days post exposure
- tissue damage
- e.g. tuberculosis, leprosy (tuberculoid), schistomiasis, sarcoidosis

23
Q

Give some examples of diseases caused by type IV hypersensitivity reactions to endogenous antigens.

A
  • pancreatic islet Cell = insulin-dependent Diabetes mellitus
  • thyroid gland = Hashimoto’s thyroiditis
  • Fc portion of IgG = rheumatoid arthritis
24
Q

What is the treatment of type III and type IV hypersensitivity reactions?

A

1) anti-inflammatory Drugs:
- non-steroidal
- corticosteroids (oral prednisolone )
- second Drugs as steroid sparing agents = azathioprine, mycophenolate mofetil, cyclophosamide

2) monoclonal antibodies:

25
Q

What is a type I hypersensitivity reaction? Give some of its characteristics.

A

Allergy

  • immunological basis for different diseases = different organs affected
  • immediate reaction (< 30 min) = local reaction (ingested/inhaled allergen), systemic reaction (insect sting or IV administration)
  • antigens (allergens) = environmental, non-infectious antigens (proteins)
26
Q

Give some examples of type 1 hypersensitivity allergens.

A
  • seasonal exposure = tree and grass pollens
  • perennial exposure = house dust mite, animal dander e.g. cats and dogs, fungal spores
  • accidental exposure = insect venom, medicines, chemicals e.g. latex, foods e.g. milk, peanuts
27
Q

What is the mechanism of a type I hypersensitivity reaction?

A
  • abnormal adaptive immune response against the allergens = T helper 2 response (IL-4, IL-5, IL-3) and IgE production
  • mast cell activation = sensitised individuals, different clinical allergic disorders depending on mast cell location
28
Q

What is the hygiene hypothesis?

A

Children exposed to animals, pets and microbes in the early postnatal period appear to be protected against certain allergic disease.

29
Q

Which cell is key in type I hypersensitivity reactions?

A

Mast cells

30
Q

What is the origin and distribution of mast cells?

A

Originate in bone marrow or other haematopoietic tissue
Locate in most mucosal and epithelial Tissues = gastrointestinal tract, skin, respiratory epithelium. In connective tissue surrounding blood cells

31
Q

Name the main mast cell mediators and their biological effects.

A
  • tryptase (enzyme) = remodel connective tissue matrix
  • histamine (toxic mediator) = toxic to parasite, increase vascular permeability, cause smooth muscle contraction
  • leukotrienes (lipid mediator) = cause smooth muscle contraction, increase vascular permeability, stimulate mucus secretion
  • platelet-activating factor (lipid mediator) = attracts leukocytes, amplifies production of lipid mediators, activates neutrophils, eosinophils and platelets
32
Q

What is the immune mechanism of an allergic reaction?

A

Allergen 1st exposure = TH2 response
Allergen 2nd exposure = IgE cross linking
Mast cell degranulation

33
Q

Give an example of a skin manifestation of allergic reaction.

A

Urticaria
Caused by mast cell activation within the epidermis
Mediators = histamine and leukotrienes/cytokines

34
Q

Give an example of a systemic manifestation of an allergic reaction. How does this occur?

A 
Anaphylaxis 
Systemic activation of mast cells:
- hypotension, cardiovascular collapse, generalised urticaria 
- angioedema 
- breathing problems
35
Q

What are the signs and symptoms of anaphylaxis?

A
  • swelling of lips, tongue, throat
  • fast/slow HR, low BP
  • hives, itchiness, flushing
  • lightheadedness, LOC, confusion, headache, anxiety
  • shortness of breath, wheeze/stridor, hoarseness, pain with swallowing, cough
  • cramps abdo pain, diarrhoea, vomiting
36
Q

What is the treatment of anaphylactic shock? What are it’s actions?

A

Epinephrine (adrenaline) IM

  • reduces peripheral vasodilation and reduces oedema and alleviates hypotension
  • reverses airway obstruction/bronchospasm
  • increases the force of myocardial contraction
  • inhibits mast cell activation
37
Q

What is allergen desensitisation?

A

Involves the administration of increasing doses of allergen extracts over a period of years, given to patients by injection or drops/tablets under the tongue (sublingual)

Immunity (4 decks)

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