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eMCD - imm > Immunology 1: Hypersensitivity + allergy > Flashcards

Immunology 1: Hypersensitivity + allergy Flashcards

1
Q

What occurs in appropriate immune reactions?

A
  • required to eliminate pathogens

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

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2
Q

What occurs in appropriate immune tolerance ?

A
  • occurs to self / foreign harmless proteins

–> Involves antigen recognition and generation of regulatory T cells and regulatory antibody (IgG4) production

e.g food, pollen

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3
Q

Hypersensitivity Reactions occur when immune responses are mounted against:

A
  • Harmless foreign antigens (allergy, contact hypersensitivity)
  • Autoantigens (autoimmune diseases)
  • Alloantigens (serum sickness, transfusion reactions, graft rejection)
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4
Q 
hypersensitivity reactions are classified by: 
Type I   : 
Type II  : 
Type III : 
Type IV :
A

Type I : Immediate Hypersensitivity
Type II : Antibody-dependent Cytotoxicity
Type III : Immune Complex Mediated
Type IV : Delayed Cell Mediated

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5
Q

give examples of allergic responses of type 1: immediate hypersensitivity

A
  • Anaphylaxis
  • Asthma
  • Rhinitis (Seasonal, Perennial)
  • Food Allergy
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6
Q

Describe the onset of Type 1 immediate hypersensitivity .

a) primary antigen exposure
b) secondary antigen exposure

A

a) primary Antigen exposure
- develop Sensitisation (not tolerance)
- involved IgE antibody production
- IgE binds to Mast Cells & Basophils

b) secondary Antigen Exposure
- More IgE Ab produced
- Antigen cross-links IgE on Mast Cells/Basophils
- -> causes Degranulation + release of inflammatory mediators

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7
Q

Clinical presentation of Type II Antibody-Dependent Hypersensitivity depends on:

A

target tissue

e.g organ specific autoimmune disease
(myasthenia gravis)

e.g autoimmune cytopenias
(hemolytic anaemia, thrombocytopenia)

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8
Q

in Type II Antibody-Dependent Hypersensitivity, what are some tests you could perform for specific autoantibodies?

A
  • Immunofluorescence
  • ELISA
  • -> e.g anti-CCP (Cyclic Citrullinated Peptide Antibodies for Rheumatoid Arthritis)
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9
Q

What happens in Type III Immune Complex Mediated Hypersensitivity ?

A
  • Formation of Antigen-Antibody complexes in blood
  • Complex deposition in blood vessels/tissue
  • leads to Complement + Cell activation
  • Activation of other cascades eg clotting
  • Tissue damage (vasculitis)
  • -> Systemic lupus erythematosus (SLE)
  • -> Vasculitides (Poly Arteritis Nodosum, many different types)
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10
Q

What are some types of type IV Delayed Hypersensitivity Responses ?

A
  • Chronic graft rejection
  • GVHD
  • Coeliac disease
  • Contact hypersensitivity
  • Many autoimmune diseases….
  • -> MOSTLY Th1 mediated
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11
Q

describe the mechanisms involved in type IV Delayed Hypersensitivity Responses.

A
  • Transient/Persistent Ag
  • T cell activation of macrophages, CTLs
  • Much of tissue damage dependent upon TNF & CTLs
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12
Q

what common features might you seen in an inflammation?

what clinical symptoms might this cause ?

A
  • increased recruitment of immune cells
  • increased activation of immune cell
  • inflammatory mediators released
  • Vasodilatation –> redness
  • Increased vascular permeability –> swelling
  • Inflammatory mediators &cytokines –> selling + pain + heat
  • Inflammatory cells & tissue damage
  • -> redness
  • -> heat
  • -> heat
  • -> pain
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13
Q 
note: 
Increased vascular permeability
Caused by:- C3a, C5a, histamine, leukotrienes
Cytokines  IL-1, IL-6, IL-2, TNF, IFN-γ
Chemokines IL-8/CXCL8, IP-10/CXCL10
Inflammatory cell infiltrate
Cell trafficking – chemotaxis
Neutrophils, macrophages, lymphocytes, mast cells
Cell activation
A

-

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14
Q

What are common allergens?

allergies = type 2 hypersensitivity

A
  • cat fur

- dust

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15
Q

What are risk factors of allergy?

A

genetic factors

  • -> polygenic risk
  • -> 80% of atopics have family history
  • -> genes on chr 11q linked to atopy + asthma
  • IL4-gene cluster linked to raise IgE, allergy

environmental factors

  • -> age
  • -> gender (more common in male children, more common in female adults)
  • -> family size
  • -> infections (early life infection protects from allergy)
  • -> animal
  • -> diet (breast feeding,fatt acids = protective)
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16
Q

What are the different types of inflammation in allergy?

A
  1. Anaphylaxis, urticaria, angioedema
    - -> type I hypersensitivity (IgE mediated)
  2. Idiopathic/chronic urticaria
    - -> type II hypersensitivity (IgG mediated)
  3. Asthma, rhinitis, eczema:
    - -> mixed inflammation
    - type I hypersensitivity (IgE mediated)
    - type IV hypersensitivity (chronic inflammation)
17
Q

Expression of disease requires what 2 aspects?

A

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

18
Q

Sensitisation in Atopic Airway Disease

A

START HERE

19
Q

Subsequent exposure

A

???

20
Q

Note: Eosinophils

Recruited during allergic inflammation

Generated from bone marrow

Nucleus - two lobes

Contain large granules
toxic proteins

Lead to tissue damage

A

-

21
Q

Crosslinking of IgE’s on mast cell surface can lead to =

A
  • Mediator release
    –> Pre-formed
    histamine + cytokines + toxic proteins
  • Newly synthesized
  • -> leukotrienes + prostaglandins
22
Q

Note: Neutrophils

  • Polymorphonuclear cells (PMNs)
  • -> nucleus contains several lobes
  • Granules contain
  • -> digestive enzymes
  • Also synthesize
  • -> oxidant radicals
  • -> cytokines
  • -> leukotrienes
A

-

23
Q

Describe the immunopathogenesis of asthma.

also, what happens in chronic inflammation of the airways

A
  • causes Acute inflammation of the airways
  • mast cell activation & degranulation
  • Pre stored mediators
    (histamine)
  • Newly synthesised mediators
    (prostaglandins+leukotrienes)
  • acute airway narrowing
QUESTION: 
Chronic inflammation of the airways
- Cellular infiltrate
(Th2 lymphocytes, eosinophils) 
- Smooth muscle hypertrophy
- Mucus plugging
 - Epithelial shedding
- Sub epithelial fibrosis
24
Q

Two-phase response to single allergen challenge

A

???

25
Q

What are 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)
26
Q

Typical day for a poorly controlled

asthmatic

A

????

27
Q

What are symptoms of allergic rhinitis?

A

Symptoms:

  • sneezing
  • rhinorrhoea
  • itchy nose, eyes
  • nasal blockage, sinusitis, loss of smell/taste
28
Q

What is allergic eczema ?

A
  • Chronic itchy skin rash
  • Flexures of arms and legs
  • 50% clears by 7 years
  • 90% by adulthood
29
Q

What happens in

a) mild food allergy
b) severe food allergy

A

Mild
- Itchy lips, mouth, angioedema, urticaria

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

30
Q

What is anaphylaxis?

A

severe generalised allergic reaction

–> causing Generalised degranulation of IgE sensitised mast cells

31
Q

what are the symptoms associatied with 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
32
Q

How would you investigate + diagnose allergic reactions?

i.e whats re the different methods

A
  • Careful history essential
  • Skin prick testing (>3mm = positive)
  • RAST (tests for IgE in the blood)
  • Total IgE
  • Lung function (asthma)
33
Q

How would you treat anaphylaxis ?

a) emergency treatment
b) prevention

A

a) Emergency Treatment:
- EpiPen & Anaphylaxis kit
- antihistamine, steroid, adrenaline
- Seek immediate medical aid

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

34
Q

How would you treat rhinitis?

A
  • anti-histamines (for sneezing, itching, rhinorrhoea)
  • nasal steroid spray (for nasal blockage)
  • cromoglycate (for children, eyes)
35
Q

How would you treat eczema ?

A

eczema = largely cell mediated

  • emollients
  • topical steroid cream
36
Q

How would you treat asthma?

A

Stage 1. Use short acting b2 agonist drugs when needed by inhalation
e.g Salbutamol

Stage 2. Inhaled steroid low-moderate dose
e.g Beclomethasone/budesonide (50-800mg per day)
Fluticasone (50-400mg per day)

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

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

37
Q

Immunotherapy

A
  • injection of allergen sensitized
  • -> start w low dose –> increase dosage overtime
  • -> useful for single antigen hypersensitivities (e.g pollen, bee stings)
  • -> SCIT (in clinic) // SLIT (at home)
  • SCIT = subcutaneous immunotherapy –> can get anaphylactic shock
  • SLIT = sublingual immunotherapy (effective against grass/pollen allergy, house dust mite)
  • -> unlikely to get anaphylactic shock
38
Q

note:

nowadays monoclonal antibodies e.g anti-IgE, anti-IL4 can be used to severe forms of disease of hypersensitivity

A

-

eMCD - imm (5 decks)

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