Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immune system > S2: hypersensitivity reactions > Flashcards

S2: hypersensitivity reactions Flashcards

1
Q

Define hypersensitivity

A

The antigen specific immune responses that are either inappropriate or excess and result in harm to host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the types of triggers for hypersensitivity

A

Exogenous – non-infectious substances, infectious microbes, drugs (penicillin)
Endogenous – infectious microbes (mimicry), self-antigens (auto-immunity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline the different types of hypersensitivity reaction

A

1) Type I or immediate (allergy) – environmental non infectious antigens
2) Type II or antibody mediated
3) Type III or immune complexes mediated
4) Type IV or cell mediated (delayed) – environmental infectious agents & self antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the two phases of the hypersensitivity reactions

A

Sensitisation phase – first encounter with the antigen, activation of APCs and memory effector cells
Effector phase – pathological reaction upon re-exposure to the same antigen and activation of the memory cells of the adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe type II hypersensitivity reactions

A 
Usually develops within 5-12 hours
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 
-physiological change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List type II hypersensitivity reactions associated with tissue/cell damage

A

Haemolytic disease of the newborn, antigen = rhesus D
Transfusion reactions, antigen = ABO system
Autoimmune haemolytic anaemia, antigen = RBCs
Immune thrombocytopenic purpura, antigen = platelets
Goodpasture’s syndrome, antigen = collagen in the glomerular basement membrane of the lung & kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe an example of a disease caused by type II hypersensitivity driven by IgM

A

Haemolytic transfusion reaction – medical emergency
-causes: errors in patient identification, improper labelling of blood specimen, testing errors etc
Incompatibility in the ABO antigens on RBCs -> donor RBC lysis induced by type II hypersensitivity involving the recipient’s IgM
Clinical outcome: shock, respiratory distress, kidney failure & death if not treated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe an example of a disease caused by type II hypersensitivity driven by IgG

A

Haemolytic disease of the newborn
1) Rh- mother carrying her first Rh+ fetus, Rh antigens from the developing fetus can enter the mother’s blood during delivery
2) In response to the fetal Rh antigens, the mother will produce anti-Rh antibodies (give RhoGAM)
3) If the woman becomes pregnant with another Rh+ fetus, her anti-Rh antibodies (IgG) will cross the placenta & damage fetal RBCs
Severe life threatening condition – hydrops fetalis, liver/splenomegaly, severe hyperbilirubinemia & kernicterus (type of brain damage that occurs with increased levels of bilirubin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List type II hypersensitivity reactions associated with physiological changes

A

Graves’ disease – increased thyroid activity, antigen = TSH receptor
Myasthenia gravis – impaired neuromuscular signalling, antigen = acetylcholine receptor
Pernicious anaemia – anaemia, antigen = intrinsic factor in gastric parietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline treatment options for type II hypersensitivity

A

Cell tissue damage – anti-inflammatory drugs, plasmapheresis, splenectomy, intravenous immunoglobulin (IVIG)
Physiological change – correct metabolism, replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe type III hypersensitivity

A

Usually develops within 3-8 hours
Involves immune complexes between IgG or IgM and antigens
Targets soluble antigens – foreign (infection), endogenous (self-antigens)
Tissue damage caused by the deposition of immune complexes in blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List key factors affecting immune complex pathogenesis

A 
Complex size
Persistence of antigen
Host response 
Local tissue factors 
Persistence if the immunocomplex & deposition drives the disease, common sites of damage -> joints, skin, small vessels & kidney = multisystem effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List examples of hypersensitivity type III reactions

A

Rheumatoid arthritis, antigen = Fc portion of IgG
Glomerulonephritis, antigen = infectious microbes
Systemic lupus erythematosus, antigen = double-stranded DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe type IV hypersensitivity

A

Usually develops within 24-72 hours
Involves lymphocytes and macrophages
Triggered by environmental factors, infectious microbes, drugs
Different subtypes – contact hypersensitivity, tuberculin hypersensitivity, granulomatous hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List diseases caused by type IV hypersensitivity to endogenous antigens

A

Insulin-dependent diabetes mellitus, antigen = pancreatic islet cells
Hashimoto’s thyroiditis, allergen = thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe treatments for type III and IV hypersensitivity

A

Anti-inflammatory and immunosuppressive drugs

Monoclonal antibodies

17
Q

List examples of allergens for type I hypersensitivity reactions

A

Seasonal exposure – tree and glass pollens
Perennial exposure – house dust mite, animal dander, fungal spores
Accidental exposure – insect venom, medicines, chemicals, foods

18
Q

Describe mechanisms of type I hypersensitivity

A

1) Abnormal adaptive immune response against the allergens – TH2 response, IgE production
2) Mast cell activation – sensitised individuals, different clinical allergic disorders depending on mast cell location (located in most mucosal & epithelial tissues, connective tissue surrounding blood cells)

19
Q

List examples of mast cell mediators

A

Enzyme – tryptase
Toxic mediator – histamine
Lipid mediator – leukotrienes C4, D4, E4, platelet-activating factor

20
Q

Outline the immune mechanism of allergic reactions

A

Allergen 1st exposure – TH2 response
Allergen 2nd exposure – IgE cross-linking
Mast cell degranulation -> increased vascular permeability, vasodilation & bronchial constriction

21
Q

Describe urticaria

A

Caused by mast cell activation within the epidermis
Mediators = histamine and leukotrienes/cytokines
If prolonged and chronic exposure = atopic dermatitis and eczema

22
Q

Describe angioedema

A

Caused by mast cell activation in the deep dermis
Mediators = histamine and bradykinin
Affects lips, eyes, tongue & upper respiratory airways

23
Q

Outline signs and symptoms of anaphylaxis

A

CNS: light-headedness, loss of consciousness, confusion, headache & anxiety
Respiratory: shortness of breath, hoarseness, cough
GI: crampy abdominal pain, diarrhoea, vomiting
Skin: hives, itchiness, flushing
Heart and vasculature: fast/slow heart rate, low BP

24
Q

State the treatment for anaphylactic shock and the mechanism of action

A

IM adrenaline
Reverses peripheral vasodilation & reduces oedema and alleviates hypotension
Reverses airway obstruction/bronchospasm
Increases the force of myocardial contraction
Inhibits mast cell activation

25
Q

List treatments for type I hypersensitivity

A 
Allergen desensitisation 
Monoclonal antibodies 
Anti-histamines 
Leukotriene receptor antagonists 
Corticosteroids
26
Q

Define 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

27
Q

What is the main pathogenic mechanism in TB?

A

Granuloma formation, which is a type IV hypersensitivity reaction
This reaction is mediated by macrophages and TH1 cells

28
Q

What are the auto-antibodies in rheumatoid arthritis?

A

Anti-cylic citrullinated peptide

Rheumatoid factor - an antibody against IgG (specifically the Fc part)

29
Q

Which cell type is responsible for:

1) the initial response in sensitisation of allergy development upon first exposure to an allergen?
2) the initial response in the effector phase upon re-exposure to an allergen?

A

1) Antigen presenting cells

2) B cells

Immune system (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions