Brainscape's Knowledge GenomeTM

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


See full index

MCD Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What do appropriate immune responses occur in response to?

A

Foreign harmful agents such as viruses, bacteria, fungi and parasites

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

What is a common side effect of an appropriate immune response?

A

Concomitant tissue damage but as long as pathogen is eliminated quickly this will be minimal and repaired easily

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

What does appropriate immune tolerance occur in response to?

A

Self and foreign harmless proteins- food, pollens, other plant proteins, animal proteins and commensal bacteria

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

What is involved in the process of immune tolerance?

A

Antigen recognition and generation of regulatory T cells and regulatory (blocking) antibody IgG4 production

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

When do hypersensitivity reactions occur?

A

When immune responses are mounted against:
Harmless foreign antigens (allergy, contact hypersensitivity)
Autoantigens (autoimmune disease)
Alloantigens (serum sickness, transfusion reactions, graft rejection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an alloantigen?

A

An antigen present only in some individuals (particular blood group) and capable of inducing the production of an alloantibody in people that lack it

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

What are the different classes of hypersensitivity?

A

Type I- immediate
Type II- Antibody-dependent cytotoxicity
Type III- Immune-complex mediated
Type IV- Delayed cell mediated

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

What does type I-III hypersensitivity depend on?

A

Interaction of antigen with antibody

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

What are common examples of type 1 hypersensitivity?

A

Anaphylaxis
Asthma
Rhinitis
Food allergy

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

What is the mechanism of type 1 hypersensitivity?

A 
1st exposure-
Sensitisation not tolerance
IgE antibody production
IgE binds to mast cells and basophils
2nd exposure-
More IgE antibody produced
Antigen cross-links IgE on mast cells and basophils
This leads to degranulation and release of inflammatory mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the clinical presentation of type 2 hypersensitivity depend on?

A

Target tissue

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

Give examples of organ specific autoimmune diseases

A 
Myasthenia gravis (anti-acetylcholine receptor antibodies)
Glomerulonephritis (anti-glomerular basement membrane antibody)
Pemphigus vulgaris (anti-epithelial cell cement protein antibody)
Pernicious anaemia (intrinsic factor blocking antibodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give some examples of autoimmune cytopenias

A

Haemolytic anaemia
Thrombocytopenia
Neutropenia

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

How can you test for specific antibodies?

A

Immunofluorescence

ELISA (anti-CCP antibodies in rheumatoid arthritis)

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

What is the mechanism of action of type 3 hypersensitivity (immune complex mediated)?

A

Formation of antigen-antibody complexes in the blood
They can’t get through small blood vessels very easily and these complexes become deposited in various tissues and lead to complement activation and cell recruitment/activation
This leads to activation of other cascades e.g. clotting which leads to:
Tissue damage, SLE and vasculitis

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

What is the most common site of vasculitis?

A

Renal (glomerulonephritis), skin, joints and lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give some examples of type 4 hypersensitivity?

A 
Chronic graft rejection
Graft-versus-host disease (GVHD)
Coeliac disease
Contact hypersensitivity
Many others- asthma, rhinitis and eczema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Th1 characterised by?

A

Producing lots of gamma-interferon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does Th2 release?

A

IL-4
IL-5
IL-13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does Th2 mediate?

A

Allergic inflammation e.g. astma, rhinitis and eczema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What do T cells activate after the antigen has come into contact?

A

Macrophages and CTLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is much of tissue damage dependent upon?

A

TNF-alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are hypersensitivity type 1-3 mediated by?

A

Antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you distinguish between type 2 and type 3?

A

Based on antigens
Type2= cell surface or matrix bound antigens
Type3= soluble antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What causes asthma?

A

IgE binding to mast cells and by the induction of T cells producing Th2 type cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the body’s response to tissue injury?

A

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the reason for inflammation?

A

It is a rapid attempt to bring body’s defences to site of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What causes inflammation?

A

Once immune cells reach the site of damage they release cytokines that leads to the features of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the features of inflammation?

A

Vasodilation- increased blood flow
Increased vascular permeability
Inflammatory mediators and cytokines
Inflammatory cells and tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the signs of inflammation?

A

Redness
Heat
Swelling
Pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What causes increased vascular permeability?

A

C3a, C5a, histamine and leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which cytokines are involved in inflammation?

A 
IL-1
IL-2
IL-6
TNF
IFN-gamma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What chemokine are involved in inflammation?

A

IL-8/CXCL8

IP-10/CXCL10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is atopy?

A

A form of allergy in which there is a hereditary of constitutional tendency to develop hypersensitivity reactions in response to allergens/ Individuals with this predisposition and conditions provoked in them by contact with allergens are described as atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How common is atopy?

A

50% of young adults in UK

36
Q

What percentage of atopics have a family history?

A

80%

37
Q

How many genes are involved in the genetic component of atopy?

A

Many- it is polygenic and 50-100 genes are associated with asthma and atopy

38
Q

Which gene cluster is linked to raised IgE, asthma and atopy?

A

IL-4 gene cluster

39
Q

Genes on which chromosome are linked to atopy and asthma?

A

Chromosome 11q (IgE receptor)

40
Q

What environmental risk factors are there for atopy?

A

Age- increases from infancy, peaks in teens and reduces in adulthood
Gender: more common in males in childhood but females in adults
Family size- more common in small families
Infections- early life infections protect
Animals- Early exposure protects
Diet- breast feeding, anti-oxidants and fatty acids protect

41
Q

What does expression of hypersensitivity disease require?

A

Development of sensitisation to allergens to sensitise instead of develop tolerance
Exposure to produce disease

42
Q

After naive CD4+T cells are activated by an antigen presenting cell they then become specific to the presented antigen and what can’t hey can then become?

A

Th1- producing IFN gamma

Th2- activation of B cells

43
Q

If a T cells is presented with a harmless antigen what can they become?

A

Regulatory T cells

44
Q

What happens in subsequent exposure when the allergens are presented by APCs to memory Th2 cells?

A

These then cause degranulation of eosinophils by releasing IL-5
Th2 cells also release IL-4 and IL-13 which stimulate the production of IgE by plasma cells
The IgE becomes mobilised onto the surface of mast cells
The antigens cross link with IgE on the surface of the mast cells and causes degranulation
There is massive release of inflammatory mediators which gives rise to allergic reaction effects

45
Q

Where are eosinophils most commonly found?

A

They are present in the blood but more reside in tissues

46
Q

When are eosinophils recruited?

A

During allergic inflammation

47
Q

What are eosinophils generated from?

A

Bone marrow

48
Q

What is the nucleus of an eosinophil like?

A

Polymorphous- two lobes

49
Q

How do eosinophils cause tissue damage?

A

They contain large granules that are full of toxic proteins

50
Q

Where are mast cells found?

A

They are tissue resident cells

51
Q

What do mast cells have on their cell surface?

A

IgE receptors

52
Q

What does cross linking of IgE with mast cells lead to?

A 
Mediator release
Preformed:
Histamine
Cytokines
Toxic proteins
Newly synthesised:
Leukotrienes
Prostaglandins
53
Q

What do all of the mediators released by mast cells cause?

A

Acute inflamation

54
Q

In terms of hypersensitivity, what are neutrophils important in?

A

Virus induced asthma, severe asthma and atopic eczema

55
Q

What percentage of blood leukocytes are neutrophils?

A

55-60%

56
Q

What do the granules in neutrophils contain?

A

Digestive enzymes

57
Q

What do neutrophils synthesise?

A

Oxidant radicals
Cytokines
Leukotrienes

58
Q

What type of hypersensitivity reaction is asthma?

A

Type 1 and 4

59
Q

What does mast cell activation and degranulation lead to?

A

Release of histamines (pre-stored mediators) and prostaglandins and leukotrienes (newly synthesised mediators)

60
Q

What does the release of mediators due to mast cell activation and degranulation lead to?

A

Acute airway narrowing

61
Q

What causes the airway narrowing in acute asthma?

A

Three processes:
Vascular leakage leading to airway wall oedema
Mucus secretion fills up the lumen
Smooth muscle contraction around the bronchi

62
Q

What is the immunopathogenesis of of chronic asthma?

A

Chronic inflammation of airways and lumen of airway is very narrow and airway wall is grossly thickened
There will be cellular infiltration- Th2 lymphocytes and eosinophils
Smooth muscle hypertrophy
Mucus plugging
Epithelial shedding
Sub-epithelial fibrosis

63
Q

What important clinical features of asthma are there?

A 
Reversible generalised airway obstruction- causes chronic episodic wheeze
Bronchial hyperresponsiveness
Cough
Mucus production
Breathlessness
Chest tightness
Response to treatment
Spontaneous variation
Reduced and variable peak expiratory flow (PEF)
64
Q

What are the two types of allergic rhinitis?

A

Seasonal- e.g. hay fever

Perennial- perennial allergic rhinitis (house dust mites, animal allergens)

65
Q

What are the symptoms of allergic rhinitis?

A

Sneezing
Rhinorrhoa
Itchy nose and eyes
Nasal blockage, sinusitis and loss of smell/taste

66
Q

How does allergic eczema present?

A

Chronic itchy skin rash

67
Q

Where is allergic eczema most commonly found?

A

Flexures of arms and legs

68
Q

What can eczema lead to?

A

House dust mite sensitisation- proteins can get through dry cracked skin

69
Q

What can complicate allergic eczema?

A

Bacteria and rarely viral infections

70
Q

What type of hypersensitivity reaction is a food allergy?

A

Type 1

71
Q

What are the most common food allergies in infants (3 years)?

A

Eggs

Cows milk

72
Q

What are the most common food allergies in children/adults?

A 
Peanuts
Shellfish
Nuts
Fruits
Cereals
Soya
73
Q

What is a mild reaction to a food allergy?

A

Itchy lips and mouth
Angioedema
Urticaria

74
Q

What is a severe reaction to a food allergy?

A

Nausea
Abdominal pain
Diarrhoea
Anaphylaxis

75
Q

What is anaphylaxis?

A

Severe generalised allergic reaction

76
Q

What happens to mast cells in anaphylaxis?

A

Generalised degranulation of IgE sensitised mast cells

77
Q

What are the symptoms of anaphylaxis?

A 
Itchiness around mouth, pharynx and lips
Swelling of lips, throat and other parts of body
Wheeze, chest tightness and dyspnoea
Faintness, collapse
Diarrhoea and vomiting
Death if severe and untreated
78
Q

What systems are affected in anaphylaxis?

A

Cardiovascular- vasodilation, cardiovascular collapse
Respiratory- bronchospasm, laryngeal oedema
Skin- vasodilation, erythema, urticaria and angioedema
GI- vomiting and diarrhoea

79
Q

How are allergies diagnosed?

A 
Careful history
Skin prick testing
RAST (radioallergosorbent test)- tests for amount of specific IgE antibodies in the blood 
Measure total IgE
Lung function (in asthma)
80
Q

How is anaphylaxis treated?

A

It is an emergency:
Epipen and anaphylaxis kit
Antihistamine if mild
Adrenaline if severe

81
Q

How are anaphylaxis attacks prevented?

A

Avoidance of allergen
Always carry epipen and anaphylaxis kits
Inform immediate family and caregivers
Wear a MedicAlert bracelet

82
Q

How do you treat allergic rhinitis?

A

Anti-histamines
Nasal steroid therapy
Cromoglycate

83
Q

How do you treat eczema?

A 
Emollients (maintain moisture in skin thus reinforcing its barrier function)
Topical steroid cream
If severe:
Anti-IgE mAb
Anti-IL4/13 mAb
Anti-IL5 mAb
84
Q

What are the 4 steps in treating asthma?

A

Step 1- short acting beta-2 agonist by inhalation e.g. salbutamol
Step 2- Inhaled steroid low-moderate dose e.g. beclomethasone/budesonide and fluticasone
Step 3- Further therapy- long-acting beta-2 agonist or leyukotrine antagonist. High dose inhaled steroid- up to 2mg a day via spacer
Step 4- Add course of oral steroids, prednisolone or anti-IgE, Anti-IL4 and anti-IL5 mAbs

85
Q

What is immunotherapy?

A

Where you make people develop tolerance but exposing them to a small amount of the allergen that they are allergic to

86
Q

Which hypersensitive is immunotherapy successful for?

A

Single antigen hypersensitivities

MCD Immunology (5 decks)

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