Brainscape's Knowledge GenomeTM

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


See full index

Immunology year 2 > Hypersensitivity and allergy > Flashcards

Hypersensitivity and allergy Flashcards

1
Q

How many of YOU have allergic sensitisation (atopy)?

A

50% of university students

However, only 30% will experience symptoms.

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

When do appropriate immune responses occur and what is the end result

A

Appropriate immune responses occur to foreign harmful agents such as viruses, bacteria, fungi, parasites
Required to eliminate pathogens
May be concomitant tissue damage as a side effect, but as long as pathogen is eliminated quickly will be minimal and repaired easily

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

What do appropriate immune responses depend on

A

Involves antigen recognition by cells of the immune system and antibody production

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

What is the function of the immune system most of the time

A

Tolerance

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

Describe appropriate immune tolerance

A

Appropriate immune tolerance occurs to self, and to foreign harmless proteins:
Food, pollens, other plant proteins, animal proteins, commensal bacteria

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

What does immune tolerance involve

A

Involves 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
7
Q

How does the immune system know whether to tolerate or respond to an antigen

A

Antigen recognition in context of “danger” signals leads to immune reactivity, absence of “danger” to tolerance

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

Ultimately, when do hypersensitivity reactions occur

A

Hypersensitivity Reactions occur when immune responses are mounted against
Harmless foreign antigens (allergy, contact hypersensitivity) i.e innocuous antigens- they would cause no damage themselves- but inappropriate immune activation leads to damage.
Autoantigens (autoimmune diseases)
Alloantigens (serum sickness, transfusion reactions, graft rejection)

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

State the Gel and Coombs classification for hypersensitivity reactions

A 
Classified by Gell & Coombs:-
Type I   : Immediate Hypersensitivity
Type II  : Antibody-dependent Cytotoxicity
Type III : Immune Complex Mediated
Type IV : Delayed Cell Mediated

Note: many diseases involve a mixture of types

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

Give an example of an all-antigen

A

Allo-antigens are antigens present in only SOME individuals (i.e. ABO blood groups).

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

Give some examples of type 1 hypersensitivity

A 
Anaphylaxis
Asthma
Rhinitis
Seasonal
Perennial
Food Allergy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define atopy and allergy

A

The immunologic definition of atopy is an immediate hypersensitivity reaction to environmental antigens mediated by IgE. Such reactions tend to run in families; these families are said to have inherited the atopy trait. Although the term allergy was originally defined as any altered reactivity to exogenous antigens, it is now often used synonymously with atopy. In this and most texts, allergy is defined as immediate hypersensitivity mediated by IgE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the pathogenesis of type 1 immediate hypersensitivity

A

10 Antigen exposure
Sensitisation not tolerance
IgE antibody production
IgE binds to Mast Cells & Basophils

20 Antigen Exposure
More IgE Ab produced
Antigen cross-links IgE on Mast Cells/Basophils
Degranulation

Degranulation leads to release of prostalgnaldins, leukotrienes, histamines (airways) which leads to the inflammation, reduction in BP and airway obstruction seen in anaphylaxis.

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

Describe how the presentation of type 2 antibody-dependent hypersensitivity depends on the target tissue

A 
Organ-specific autoimmune diseases
Myasthenia gravis (Anti-acetylcholine R Ab)
Glomerulonephritis (Anti-glomerular basement membrane Ab)
Pemphigus vulgaris (Anti-epithelial cell cement protein Ab)
Pernicious anaemia (Intrinsic factor blocking Abs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the autoimmune cytopenias associated with type 2 hypersensitivity reactions

A

Autoimmune cytopenias (Ab mediated blood cell destruction)
Haemolytic anaemia
Thrombocytopenia
Neutropenia

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

Describe how we can test for specific autoantibodies in type 2 hypersensitivity reactions

A

Test for specific autoantibodies
Immunofluorescence
ELISA eg anti-CCP (Cyclic Citrullinated Peptide Abs for Rheumatoid Arthritis)

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

What are the key features of immune-mediated hypersensitivity (type 3)

A

Formation of Antigen-Antibody complexes in blood
Complex deposition in blood vessels/tissue
Complement & cell activation
Activation of other cascades eg clotting
Tissue damage (vasculitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

State some common examples of type 3 hypersensitivity reactions

A

Systemic lupus erythematosus (SLE)

Vasculitides (Poly Arteritis Nodosum, many different types)

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

Where is vasculitis common in type 3 hypersensitivity

A 
Vasculitis:
Renal (glomerulonephritis) 
Skin
Joints
Lung

Immune complex deposits in blood vessels in these regions- leading to complement activation, recruitment of monocytes and neutrophils — inflammation

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

What are the Th1 mediated type 4 delayed type hypersensitivity reactions

A 
Chronic graft rejection
GVHD
Coeliac disease
Contact hypersensitivity
Many autoimmune diseases….
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the Th2 mediated type 4 hypersesensitivity reactions

A

Asthma
Rhinitis
Eczema

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

What are the different types of Type 4 hypersensitivity reactions

A

Th1
Cytotoxic
Th2

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

Summarise the mechanisms of type 4 hypersensitivity

A

Transient/Persistent Ag
T cell activation of macrophages, CTLs
Much of tissue damage dependent upon TNF & CTLs

APC presents antigen to Th1 cell
Th1 releases IL-2 to activate CTLs which release perforin to kill cells
Th1 also releases IFN-y to activate macrophages, which releases TNF to kill cells
In chronic reactions- Th1 will also release FGF to activate fibroblasts, which leads to angiogenesis and fibrosis.

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

Describe a common example of cell-mediated type 4 hypersensitivity

A

Nickel

Contact Hypersensitivity

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

What is a common feature of the hypersensitivity reactions

A

Common Feature – inflammation
Immune cell
recruitment to sites of injury and/or infection
activation
Inflammatory mediators – complement, cytokines, etc

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

What are the key features of inflammation

A

Vasodilatation, increased blood flow
Increased vascular permeability
Inflammatory mediators & cytokines
Inflammatory cells & tissue damage

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

What are the key signs of inflammation

A

Redness
Heat
Swelling
Pain

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

What are the key mediators of inflammation

A

Increased vascular permeability
Caused by:- C3a, C5a, histamine, leukotrienes

Cytokines IL-1, IL-6, IL-2, TNF, IFN-γ

Chemokines IL-8/CXCL8 (neutrophils), IP-10/CXCL10 (lymphocytes)

Inflammatory cell infiltrate
Cell trafficking – chemotaxis
Neutrophils, macrophages, lymphocytes, mast cells
Cell activation

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

Summarise allergy

A 
Common - prevalence of atopy is 50% in young adults in UK
Severity varies -
mild occasional symptoms
severe chronic asthma
life threatening anaphylaxis
Risk factors - genetic and environmental
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the genetic risk factors for allergy

A

~80% of atopics have a family history
Polygenic
50-100 genes linked to asthma/atopy
genes of IL-4, 5, 13 gene cluster (chromosome 5) linked to raised IgE, asthma, atopy
genes on chromosome 11q (IgE receptor) linked to atopy and asthma
genes linked to structural cells linked to eczema (filaggrin) and asthma (IL-33, ORMDL3, CDHR3)

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

Describe the environmental risk factors for allergy

A

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

32
Q

What is happening to the prevalence in allergies in the UK

A

Increasing yearly

Indicates change in environment playing a major role- genetic won’t have had time to influence change in suceptibility

33
Q

Summarise the different types of inflammation in allergy

A

Anaphylaxis, urticaria, angioedema
type I hypersensitivity (IgE mediated)

Idiopathic/chronic urticaria
type II hypersensitivity (IgG mediated)

Asthma, rhinitis, eczema:
mixed inflammation
type I hypersensitivity (IgE mediated)
type IV hypersensitivity (chronic inflammation)

34
Q

What is key for the expression of allergic disease

A

Development of sensitisation to allergens instead of tolerance (primary response - usually in early life)
Further allergen exposure to produce disease (memory response - any time after sensitisation)

35
Q

Describe sensitisation in allergic airway disease

A

Allergen comes into contact with the ciliated epithelium of the lungs
Dendritic cell underling the epithelium process the allergen and presents it to CD4+ T cells
Instead of differentiating into T-reg, which would induce tolerance, they differentiate into Th2
Th2 activate B cell proliferation and differentiation (via IL-4 and IL-13) into plasma cells which synthesise and release IgE (switch from IgG)

36
Q

Describe what happens upon second exposure to the antigen in allergic airway disease

A

In second exposure, the allergens are presented by APCs to memory Th2 cells, which then release IL-5, which causes eosinophil degranulation
Th2 cells also release IL-4 and IL-13, which stimulate production of IgE by plasma cells
The antigens crosslink the IgE on the surface of mast cells causing degranulation

Eosinophils and mast cells release the mediators of inflammation

37
Q

Summarise the key features of eosinophils

A

0-5% of blood leukocytes

Present in blood, most reside in tissues

Recruited during allergic inflammation

Generated from bone marrow

Nucleus - two lobes

Contain large granules
toxic proteins

Lead to tissue damage

Treatments that prevent the activation of eosinophils effective at treating allergic diseases

38
Q

Summarise the key features of mast cells

A

Tissue resident cells

IgE receptors on cell surface

 Crosslinking of IgEs leads to
Mediator release
Pre-formed
histamine
cytokines
toxic proteins
Newly synthesized
leukotrienes
prostaglandins
39
Q

Summarise neutrophils

A

Important in
virus induced asthma
severe asthma
atopic eczema

55-70% of blood leukocytes
Polymorphonuclear cells (PMNs)
nucleus contains several lobes

Granules contain
digestive enzymes

Also synthesize
oxidant radicals
cytokines
leukotrienes

40
Q

Summarise the acute phase of the immunopathogenesis of asthma

A

Acute inflammation of the airways
mast cell activation & degranulation

Pre stored mediators
histamine

Newly synthesised mediators
prostaglandins, leukotrienes

acute airway narrowing
due to :
smooth muscle contraction - leukotrienes
mucus secretion -leukotrienes
vascular leakage and thus airway wall oedema

all these obstruct the lumen of the airways – bronchoconstriction

41
Q

Describe the two phase response to the single allergen challenge

A

Asthmatic
Baseline- PEF already slightly low due to tonic bronchoconstriction

Inhale allergen (e.g dust) - early response- acute and dramatic decrease in PEF- due to mast cell degranulation

Then get a late response a couple of hours later- due to cellular response- Type 4- eosinophils, lymphocytes, neutrophils etc – constantly inhaling allergen- so risk always present to some degree

42
Q

Summarise the immunopathogensis of the late phase of asthma

A 
Chronic inflammation of the airways
Cellular infiltrate
Th2 lymphocytes, eosinophils
Smooth muscle hypertrophy
Mucus plugging
Epithelial shedding
Sub epithelial fibrosis

Mediators released by eosinophils include peroxidase, eosinophil major basic protein, and cationic protein, which all cause direct damage to bronchial tissue. As a result of the chronic allergic inflammation, the bronchial smooth muscle is hypertrophic, and mucus secretion is increased; airflow becomes persistently, rather than intermittently, reduced.

43
Q

Summarise the key clinical features of asthma

A

Reversible generalised airway obstruction
Chronic episodic wheeze

Bronchial hyperresponsiveness
Bronchial irritability

Cough
Mucus production
Breathlessness
Chest tightness

Response to treatment
Spontaneous variation
Reduced & variable peak flow (PEF)

Reversible and episodic nature important in diagnosis

44
Q

When may an asthmatic take their reliever inhaler

A

Upon symptoms- don’t prevent attacks- just treats them as they occur

45
Q

What are the two different types of allergic rhinitis

A

Seasonal - hay fever - grass, tree pollens

Perennial - perennial allergic rhinitis
HDM, pets

46
Q

What are the symptoms of allergic rhinitis

A 
Symptoms
sneezing
rhinorrhoea
itchy nose, eyes
nasal blockage, sinusitis, loss of smell/taste

In severe cases- may have nasal polyps

47
Q

Describe the key features of allergic eczema

A 
Chronic itchy skin rash
Flexures of arms and legs
HDM sensitisation and dry cracked skin
Complicated by bacterial and (rarely) viral infections (early childhood, herpes simplex)
50% clears by 7 years
90% by adulthood
48
Q

Summarise the difference in food allergies between adults and infants

A

Infancy-3yrs
egg, cows milk

Children/adults
peanut, nuts, shell fish, fruits, cereals, soya

49
Q

Describe the different reaction types to food allergies

A

Mild
Itchy lips, mouth, angioedema, urticaria

Severe
Nausea, abdominal pain, diarrhoea, collapse, wheeze
Anaphylaxis

Collapse- due to vasodilation- loss of blood pressure

50
Q

Essentially, what is meant by anaphylaxis

A

Anaphylaxis: severe generalised allergic reaction
Uncommon, potentially fatal
Generalised degranulation of IgE sensitised mast cells

51
Q

Describe the symptoms of anaphylaxis

A 
Symptoms:
itchiness around mouth, pharynx, lips
swelling of the lips, throat and other parts of the body
wheeze, chest tightness, dyspnoea
faintness, collapse
diarrhoea & vomiting
death if severe & untreated
52
Q

Describe the different systems involved in anaphylaxis

A

Systems:
Cardiovascular - vasodilatation, cardiovascular collapse
Respiratory - bronchospasm, laryngeal oedema
Skin - vasodilatation, erythema, urticaria, angioedema
GI - vomiting, diarrhoea- due to vascular leakage and oedema of G.I tract

53
Q

Describe the different investigations used in the diagnosis of anaphylaxis

A 
Careful history essential
Skin prick testing
RAST (blood specific IgE):
Total IgE
Lung function (asthma)

RAST= • RAST (radioallergosorbent test) – tests the amount of specific IgE antibodies in the blood
Place allergen on membrane- place sample of patient’s blood on membrane- radioisotope will bind to IgE bound to the allergen.

54
Q

Describe the emergency treatment of anaphylaxis

A

Emergency Treatment
EpiPen & Anaphylaxis kit
antihistamine, steroid, adrenaline
Seek immediate medical aid

55
Q

Describe the prevention of anaphylaxis

A 
Prevention
Avoidance of known allergen
Always carry a kit & EpiPen
Inform immediate family & caregivers
Wear a MedicAlert® bracelet
56
Q

Summarise the treatment for allergic rhinitis

A

anti-histamines (sneezing, itching, rhinorrhoea)
nasal steroid spray (nasal blockage)- better for perennial- anti-histamines ineffective at preventing nasal blockage
cromoglycate (children, eyes)- mast cell inhibitor

57
Q

Summarise the treatment for eczema

A

emollients- to thicken the skin barrier

topical steroid cream

58
Q

generally, what can be used to treat severe hypersensitivity reactions

A

If severe
anti-IgE, anti-IL-4/-13, anti-IL-5 mAb
anti IL-5- will prevent activation and recruitment of eosinophils

59
Q

Describe the stepwise asthma treatment

A

Step 1. Use short acting b2 agonist drugs as required by inhalation
Salbutamol - if mild and intermittent - don’t prevent

Step 2. Inhaled steroid low-moderate dose
Beclomethasone/budesonide (50-800mg per day)
Fluticasone (50-400mg per day) used to prevent

Step 3. Add further therapy
Add long acting bronchodilators, leukotriene antagonist
High dose inhaled steroids - up to 2mg per day via a spacer

Step 4. Add courses of oral steroids, SLIT, azithromycin
Prednisolone 30mg daily for 7-14 days
Anti-IgE, anti-IL-5, anti-IL-4/-13 monoclonal Abs

more severe as you go down

60
Q

When is immunotherapy effective

A 
Effective for single antigen hypersensitivities
Venom allergy - bee or wasp stings
Pollens
HDM
Antigen used is purified
61
Q

Describe subcutaneous immunotherapy

A

Subcutaneous immunotherapy (SCIT)
3 years needed
Weekly/monthly 2hr clinic visits

designed to induce tolerance - not sensitisation

done in clinic- in case of sever anaphylactic reaction

62
Q

Describe sublingual immunotherapy

A

Sublingual immunotherapy (SLIT)
Can be taken at home
3yrs needed

63
Q

When does allergy occur

A

Allergy occurs when a damaging immune response develops to an otherwise innocuous foreign substance, the antigen involved is referred to as the allergen.

Most allergic disease is produced by mixed type I and type IV hypersensitivity reactions.

Type I is immediate hypersensitivity/IgE- mediated

Type IV is cell mediated chronic inflammation

64
Q

What is the difference between allergy and atopy

A

Atopy is the tendency to produce abnormally high IgE responses to otherwise harmless foreign environmental substances.

Allergic disease is the expression of a disease caused by atopy

65
Q

Summarise the immunopathogenesis of allergic disease

A

Specific IgE produced on first exposure
IgE binds to Fc receptors on mast cells
Re-exposure to allergen cross-links IgE with mast cell activation (synthesis of prostaglandins/leukotrienes) and degranulation (histamine and other mediators) produce vasodilation, and permeability of blood vessels with fluid entering mucosal tissues with swelling (oedema), increased mucus secretion (rhinorrhoea, sputum production), neural stimulation (cough, sneezing, itch).
Chronic inflammation with lymphocyte and eosinophil activation and infiltration

66
Q

Describe the clinical manifestation of different organs in response to allergens

A

nose allergic rhinitis inhaled
bronchi allergic asthma inhaled
blood circulation anaphylactic shock oral/mucosal contact/inhaled
skin allergic eczema skin contact

67
Q

What is allergic rhinitis often associated with

A

often associated with: sinusitis, otitis media, allergic conjunctivitis, asthma

68
Q

What is the prevalence of asthma in the U.K

A

Asthma is common (4-20% UK population)

69
Q

What factors can precipitate an acute asthma attack

A

Factors that may precipitate acute attack of asthma:

Viral infectionAllergen exposureCold air / Exercise
Irritants
Emotional stress

70
Q

State the common causes of anaphylaxis

A

Bee and wasp stings ie venom allergy

Food e.g. peanut allergy, shellfish, fruits and vegetables

Drug allergy e.g. penicillin

Where allergen is introduced directly into the blood e.g. bee sting, the reaction can be almost instantaneous with cardiovascular collapse the predominant feature.

Where the allergen is absorbed through skin or mucosa e.g. peanut allergy, the reaction may develop more slowly, but is still very rapid.

Milder forms of urticaria/angioedema much more common that full anaphylaxis.

71
Q

Describe anaphylactoid reactions

A

Anaphylactoid/anaphylaxis-like reactions are clinically identical to anaphylaxis but the mast cell activation is not due to IgE-mediated allergy. No prior exposure is required. A number of other mast cell triggers may operate instead e.g. complement activation by radiocontrast media, direct stimulation of mast cells by opiates, alcoholic drink constituents or food colours e.g. tartrazine.

The treatment of the acute episode is the same

72
Q

Summarise the investigations and diagnosis of allergy

A

Careful history is essential
Immediate hypersensitivity (type I) skin prick tests very useful to confirm presence of atopy and identify possible causative allergens
Specific IgE measurement (RAST) only necessary if:
On antihistamines
Extensive skin disease
Presence of dermatographism
Very young baby
Previous anaphylaxis
Skin test solution not available
Challenge with allergen e.g. for food allergy, occupational allergy
Other tests e.g. total IgE, lung function tests for asthma

73
Q

What is the immune reactant in type 2 hypersensitivity

A

IgG
Responds to either:

cell or matrix antigen – complement , macrophages, NK cells - -some drug allergies (penicillin)
cells surface receptor – antibody alters signalling- chronic urticaria

74
Q

What is the immune reactant in type 3 hypersensitivity

A

IgG
Responds to soluble antigen – complement and phagocyte activation

serum sickness, Arthur reaction

75
Q

Describe the different types of type 4 hypersensitivity

A

Th1 - soluble antigen - macrophage activation - contact dermatitis, TB

Th2- soluble antigen - eosinophil activation - chronic asthma and allergic rhinitis

CTL - cell-associated antigen - cytotoxicity - contact dermatitis

Immunology year 2 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions