Brainscape's Knowledge GenomeTM

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


See full index

Year 2: MCD > Immunology 1: Hypersensitivity and allergy > Flashcards

Immunology 1: Hypersensitivity and allergy Flashcards

1
Q

Describe an appropriate immune reaction

A

Immune responses occur to foreign harmful agents e.g viruses, bacteria. etc. Antigen recognition by cells of the immune system –> antibody production

Immune response will:

  • Eliminate pathogens
  • may cause tissue damage as a side effect (but as long as the pathogen is eliminated it will be repaired easily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a hypersensitivity reaction?

A

Occurs when immune responses are mounted against:

  • Harmless foreign antigens (allergy, contact hypersensitivity)
  • 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
3
Q

What are the classifications of hypersensitivity reactions?

A

Type I: Immediate Hypersensitivity
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
4
Q

Give examples of type I hypersensitivity reactions

A

Type I: immediate hypersensitivity

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

Describe primary antigen exposure in type I hypersensitivity?

A

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

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

Describe secondary antigen exposure in type I hypersensitivity?

A

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

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

What are the two types of type II hypersensitivity?

A

Organ specific autoimmune disease

  • 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)

Autoimmune cytopenias

  • Haemolytic anaemia
  • Thrombocytopenia
  • Neutropenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you test for specific autoantibodies?

A

This is used for type II hypersensitivity

  • Immunofluoresence
  • 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
9
Q

Describe the process of the type III hypersensitivity

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)
    1) Systemic lupus erythematosus (SLE)
    2) Vasculitides (Poly Arteritis Nodosum, many different types)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type III Immune Complex Mediated Hypersensitivity
Slide 15

A

???

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

Give examples of type IV hypersensitivity responses?

A
  • Chronic graft rejection
  • GVHD
  • Coeliac disease
  • Contact hypersensitivity
  • Many autoimmune diseases….
  • Asthma
  • Rhinitis
  • Eczema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three main varieties of type IV delayed hypersensitivity responses?
Describe the mechanisms?

A

Th1
Cytotoxic
Th2

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

See slides

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

How does inflammation arise?

A

Common feature of immune responses

Immune cell - recruited to sites of injury and/or infection. Activated
Inflammatory mediators - Complement, cytokines etc.

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

What are the features of inflammation?

A

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

Signs:

  • redness
  • heat
  • swelling
  • pain

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
15
Q

What causes the increased vascular permeability in inflammation?

A

C3a, C5a, histamine and leukotrienes

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

What cytokines are released in inflammation?

A

IL-1, IL-6, IL-2, TNF, IFN-gamma

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

What chemokines are released in inflammation?

A

IL-8/CXCL8, IP-10/CXCL10

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

What are the risk factors for allergy?

A

Genetic and environmental

Genetic - polygenic.
Genes on IL-4 gene cluster = raised IgE, asthma, atopy
Genes on chr. 11q (IgE receptor) = Asthma and atopy
Genes linked to structural cells = eczema

Environmental:

  • Age
  • Gender
  • Family size
  • Infection
  • Animals
  • Diet

Allergy risk in the UK is increasing.

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

What are the levels of allergy severity?

A
  • Mild occasional symptoms
  • Chronic asthma
  • Life threatening anaphylaxis
20
Q

What are the 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:
    1) type I hypersensitivity (IgE mediated)
    2) type IV hypersensitivity (chronic inflammation)
21
Q

What does the expression of disease require?

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)

22
Q

Define atopy

A

Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema).

23
Q

Describe the sensitisation of atopic airway disease?

A

See slides

24
Q

What do eosinophils contain?

A

Large granules –> toxic proteins

Leads to tissue damage. They are recruited to allergic inflammation

25
Q

Describe 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
26
Q

What allergies are neutrophils important in?

A

virus induced asthma
severe asthma
atopic eczema

27
Q

What do the granules of neutrophils contain and what can they synthesize?

A

Digestive enzymes

Synthesize:

  • oxidant radicals
  • cytokines
  • leukotrienes
28
Q

Define acute asthma?

A

Acute inflammation of the airway:

Mast cell activation & degranulation

Pre stored mediators released:
- histamine

Newly synthesised mediators
- prostaglandins, leukotrienes

Acute airway narrowing

29
Q

What is the two-phase response to single allergen challenge?

A

See slides

30
Q

Describe the immunopathogenesis of chronic asthma

A

Chronic inflammation of the airways.

1) Cellular infiltrate
- Th2 lymphocytes, eosinophils
2) Smooth muscle hypertrophy
3) Mucus plugging
4) Epithelial shedding
5) Sub epithelial fibrosis

31
Q

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)

32
Q

Describe allergic rhinitis

A

Seasonal - hay fever - grass, tree pollens

Perennial - perennial allergic rhinitis
- HDM, pets

Symptoms:

  • sneezing
  • rhinorrhoea
  • itchy nose, eyes
  • nasal blockage, sinusitis, loss of smell/taste
33
Q

Describe 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
34
Q

Describe mild and severe food allergy

A

Mild
- Itchy lips, mouth, angioedema, urticaria

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

35
Q

What can cause food allergies in infancy?

A

Egg, cows milk

36
Q

What can cause food allergies in children/adults?

A

Peanuts, nuts, shell fish, fruits, cereals, soya

37
Q

What is anaphylaxis?

A

Severe generalised allergic reactions. It is uncommon but potentially fatal.

Generalised degranulation if IgE sensitised mast cells.

38
Q

What are the symptoms of anaphylaxis?

A
  • 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
39
Q

What systems are affected in anaphylaxis?

A

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

40
Q

How do you investigate and diagnose allergies?

A 
Careful history essential
Skin prick testing
RAST (blood specific IgE):
Total IgE
Lung function (asthma)
41
Q

What is the emergency treatment of anaphylaxis?

A

EpiPen & Anaphylaxis kit

  • antihistamine, steroid, adrenaline
  • Seek immediate medical aid
42
Q

How do you prevent anaphylaxis?

A

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

43
Q

How do you treat allergic rhinitis?

A
  • anti-histamines (sneezing, itching, rhinorrhoea)
  • nasal steroid spray (nasal blockage)
  • cromoglycate (children, eyes)

If severe: anti-IgE, anti-IL-4/-13, anti-IL-5 mAb

44
Q

What is the treatment for Eczema?

A
  • Emollients
  • Topical steroid cream#

If severe: anti-IgE, anti-IL-4/-13, anti-IL-5 mAb

45
Q

What is the asthma treatment plan?

A

See slide 47

Year 2: MCD (40 decks)

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