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Year 2 Collin > Immune 1 - Hypersensitivity and Allergy > Flashcards

Immune 1 - Hypersensitivity and Allergy Flashcards

1
Q

What are the 4 types of hypersensitivity

A

Type 1: Immediate hypersensitivity (IgE mediated)
Type 2: Antibody-dependent cytotoxicity
Type 3: Immune complex mediated
Type 4: Delayed cell mediated

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2
Q

Type 1 hypersensitivity (immediate) involves which forms of allergY

A
  1. Anaphylaxis
  2. Asthma
    3, Rhinitis (seasonal and perennial)
  3. Food allergy
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3
Q

Explain how immediate hypersensitivity works

A

Initial antigen exposure:

  1. Sensitation occurs (not tolerance)
  2. IgE antibody production
  3. IgE binds to mast cells and basophils

Secondary antigen exposure:

  1. More IgE antibody produced
  2. Antigen crosslinks IgE on mast cells/basophils
  3. Degranulation and release of mediators
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4
Q

Describe some organ specific presentations of Type 2 (antibody dependent hypersensitivity)

A
  1. Myasthenia graves (anti-ACh receptor Ab)
  2. Glomerulonephritis (anti-glomerular basement membrane Ab)
  3. Pemphigus vulgaris (anti-epithelial cell cement protein Ab)
  4. Pernicious anaemia (intrinsic factor blocking Ab)

Can also get autoimmune cytopenias

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5
Q

What tests can be done for specific antibodies?

A
  1. Immunofluorescence

2. ELISA (e.g. anti-CCP Abs for rheumatoid arthritis)

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6
Q

Explain how Type 3 hypersensitivity works (Immune complex mediated)

A
  1. Antigen-Ab complex forms in blood
  2. Complex deposition in blood vessels/tissue
  3. Complement and cell activation at site of deposition
  4. Activation of other cascades (e.g. clotting)
  5. Tissue damage (vasculitis)

Common sites of vasculitis = lungs, skin, joints, renal

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7
Q

Which diseases are based of type 3 hypersensitivity?

A

SLE, vasculitides (polyarteritis nodosum)

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8
Q

Describe some type 4 sensitivity disorders (delayed hypersensitivity)

A
  1. Chronic graft rejection
  2. GVHD
  3. Coeliac disease
  4. Contact hypersensitivity
  5. Autoimmune diseases

All above are Th1 mediated

Asthma, rhinitis and eczema are Th2 mediated and can be type 4 too

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9
Q

In type 4, much of the tissue damage is dependent on?

A

TNF and CTLs

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10
Q

What are the signs of inflammation

A

Redness, heat, swelling, pain

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11
Q

What contributes to the increased vascular permeability in inflammation.

What are the important cytokines

What are the important chemokines

A

Increased vascular permeability:
C3a, C5a, histamine and leukotrienes

Cytokines: IL1, IL6, IL2, TNF, IFN-y

Chemokines: IL8, IP-10

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12
Q

What are chemokines

A

Cytokines that attract inflammatory cells

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13
Q

Which immune cells are important in inflamamtion

A

Neutrophils, macrophages, lymphocytes and mast cells (but mast cells = th2 activated)

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14
Q

Allergy has a polygenic component - explain

A
  1. Genes of IL4 cluster on Chr 5 linked to raised IgE, asthma, atopy
  2. Genes on Chr 11q (IgE receptor) linked to atopy and asthma
  3. Genes linked to structural cells linked to eczema (filaggrin) and asthma (IL-33, ORMDL3, CDHR3)
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15
Q

Describe some environmental risk factors for allergy

A 
Age
Gender
Family size
Infections (early infections protect)
Animals
Diet
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16
Q

Type 1 hypersensitivity is IgE mediated. What Ig mediates Type 2

A

IgG

17
Q

Describe the types of inflammation in allergy

A

Type 1 (IgE): anaphylaxis, urticaria, angioedema

Type 2 (IgG): idiopathic/chronic urticaria

Asthma, rhinitis, eczema = mixed inflammation from Type1 hypersensitivity and type 4 hypersensitivity (Type 4 = th2 driven)

18
Q

Where do most eosinophils reside

A

In tissue - they are recruited in allergic inflammation

Bilobed nuclei

Eosinophils contain large granules w/ toxic proteins) - leads to tissue damage

19
Q

What receptors do mast cells have on their surface

A

IgE

Crosslinking of Mast cells and IgEs leads to mediator release

Mediator release involves preformed histamine/cytokine/toxic protein and newly synthesised leukotrienes and prostaglandins

20
Q

Neutrophils make up 55-70% of blood leukocytes - and have polymorphonuclear cells. When are they important?

What can they synthesise

A

Important in virus induced asthma, severe asthma, atopic eczema

Their granules contain digestive enzymes

Neutrophils can also synthesise oxidant radicals, cytokines, leukotrienes

21
Q

Describe the acute immunopathogenesis of asthma

A

Acute inflammation of the airways

Mast cell activation and degranulation releases mediators

The mediators cause acute airway narrowing by causing: Airway wall oedema, mucus secretion and SM contraction

22
Q

Describe the chronic immunopathogenesis of asthma

A

Chronic inflammation of the airways

Cellular infiltrate including Th2 lymphocytes and eosinophils

Smooth muscle hypertrophy, mucus plugging, epithelial shedding, sub epithelial fibrosis

23
Q

What are the clinical features of asthma

A
  1. Reversible generalised airway obstruction (chronic episodic wheeze)
  2. Bronchial hyper responsiveness (bronchial irritability)
  3. Cough
  4. Mucus production
  5. Breathlessness
  6. Chest tightness

they respond to treatment, have spontaneous variation and reduced/variable peak flow

24
Q

Describe allergic eczema

A

Chronic itchy skin rash on flexures of arm and legs

House dust mite sensitisation and dry, cracked skin

Complicated by bacterial and viral (rare) infections

90% clears by adulthood

25
Q

Describe anaphylaxis

A

Severe generalised allergic reaction - caused by generalised degranulation of IgE sensitised mast cells

26
Q

Describe investigation and diagnosis of allergy

A
  1. Careful history
  2. Skin prick testing
  3. RAST (blood specific IgE)
  4. Total IgE
  5. Lung function (Asthma)
27
Q

What is the treatment of anaphylaxis

A

Emergency : epipen and anaphylaxis kit (antihistamine, steroid, adrenaline + seek immediate medical aid)

Prevention: avoid allergen, carry epipen, inform immediate family and caregivers, wear medic alert bracelet

28
Q

What is the treatment for allergic rhinitis

A
  1. Anti-histamines (treats sneezing, itching, rhinorrhoea)
  2. Nasal steroid spray (nasal blockage)
  3. Cromoglycate (prevents degranulation)
29
Q

What is the treatment for eczema

A
  1. Emollients
  2. Topical steroid cream

If severe- anti-IgE, anti-IL4/13, anti-Il5 mAb

30
Q

Describe asthma treatment

A

Step 1: short acting B2 agonist drug (salbutamol)

Step 2: Inhaled steroid (beclomethasone/budesonide)

Step 3: Long acting bronchodilators (leukotriene antagonist) / high dose inhaled steroids

Step 4: Add courses of oral steroids, SLIT, azithromycin (prednisolone), anti-IgE, anti-Il5, Anti-il4/13 mAbs

31
Q

Describe immunotherapy

A

Useful for single antigen hypersensitivities (e.g. venom, pollens, dust mites)

Subcutaneous immunotherapy (SCIT) - done for 3 years

Sublingual immunotherapy (SLIT) - can be taken at home, 3 years

Year 2 Collin (114 decks)

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