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Immuno > 1: Hypersensitivty and allergy > Flashcards

1: Hypersensitivty and allergy Flashcards

1
Q

When do hypersensitivity reactions occur?

A

Occur when immune responses are mounted against

  • Harmless foreign antigens
  • Autoantigens
  • Alloantigens
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2
Q

What are the 4 types of hypersensitivity reactions?

A

Type 1 = IMMEDIATE hypersensitivity
Type 2 = Antibody-dependent Cytotoxicity
Type 3 = Immune complex mediated
Type 4 = Delayed Cell Mediated

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3
Q

What is type 1 hypersensitivity? Give clinical examples

A

Anaphylaxis, asthma, rhinitis, food allergy

1st antigen exposure: Develop sensitivity, NOT tolerance
IgE produced, binds to mast cells & basophils

2nd antigen exposure: MORE IgE produced, antigen CROSS-LINKS IgE molecules on mast cells/basophils, leading to DEGRANULATION

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4
Q

What is type 2 hypersensitivity? Give clinical examples

A

Auto-antibodies

Clinical presentation depends on target tissue

Organ-specific autoimmune diseases - Myasthenia Gravis (Ab to Ach receptors) , Pemphigus vulgaris (Ab to epithelial cell cement protein)

Autoimmune cytopenias - haemolytic anaemia, thrombocytopenia, neutropenia

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5
Q

Tests for antibodies?

A

Immunoflourescence

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

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6
Q

What is type 3 hypersensitivity? Give clinical examples

A

Antigen-antibody complexes in blood get deposited in blood vessels/tissues and leads to complement/cell activation (+clotting)
Results in TISSUE DAMAGE (Vasculitis)

SLE (lupus)
Other vasculitides

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7
Q

What is type 4 hypersensitivity? Give clinical examples

A

Antigens presented by antigen presenting cells to Th1 lymphocytes
Th1 produces interferon gamma (IFN gamma)
Activates macrophages that release Tumour necrosis factor (TNF)
Activates fibroblasts causing angiogenesis/fibrosis
Activates Cytotoxic T lymphocytes (CTL) by production of IL-2.
Most tissue damage from CTL + TNF

Th1 mediated:
Chronic graft rejection
GVHD
Coeliac disease
Contact hypersensitivity (skin)
Many autoimmune diseases

Th2 mediated:
Asthma, rhinitis, eczema

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8
Q

Features of inflammation

Give examples of mediators

A

Vasodilation
Increased vascular permeability (caused by complement activation/histamine release)
Inflammatory mediators/cytokines (IL-1/2/6, TNF, IFNgamma)
Inflammatory cells + tissue damage

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9
Q

Main cells involved in inflammation?

A

Neutrophils, macrophages, lymphocytes, mast cells

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10
Q

Prevalence of atopy in UK?

A

50%

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11
Q

Genetic risk factors of allergy?

A

80% of atopics have family history
Polygenic (many genes linked to asthma/atopy)

Examples of genes:

  • IL-4 gene cluster (linked to raised IgE)
  • Genes on chromosome 11q (IgE receptor)
  • Genes linked to structural cells (filaggrin linked to eczema, IL-33 linked to asthma)
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12
Q

Environmental risk factors of allergy?

A
  1. Age - increases in infancy, peaks in teens, decreases in adulthood

2.Childhood - more common in males
Adulthood - more common in females

  1. More common in small families
  2. Early life infections protect from allergy
  3. Animals - early exposure protects from allergy
  4. Diet (anti-oxidants/breast-feeding, fatty acids protect)
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13
Q

Prevalence of allergies in UK?

A

Asthma, eczema, hay fever all RISING

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14
Q

Types of inflammation?

A

Asthma, rhinitis, eczema = MIXED inflammation (type 1+4 hypersensitivity) so both IgE mediated and chronic inflammation

Anaphylaxis, urticaria, angiodema = Type 1 hypersensitivity (IgE mediated)

Idiopathic/chronic urticaria = Type 2 (IgG mediated)

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15
Q

What does expression of these diseases require?

A

Primary response (early life) = Development of SENSITISATION to allergens rather than tolerance

Memory/secondary response = FURTHER allergen exposure causing disease

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16
Q

Explain the process of an allergic reaction

A

Allergen sampled by dendritic cells in epithelial layer
Dendritic cells processes allergen and presents peptides to naive T cell
Naive T cells differentiate into Th2 cells to produce allergic response (Th1 = autoimmune, regulatory T cells = tolerance)
Th2 proliferate and release IL-4/13 that signal B cells to produce IgE
IgE binds to plasma cells

On second exposure:
Processed allergen presented to memory Th2 cells
Leads to more IgE production
Antigens bind to IgE on MAST CELLS, causing degranulation of inflammatory mediators

Th2 also release IL-5 which activates EOSINOPHILS

17
Q

Structure of eosinophils?

A

Mostly reside in tissues, some in blood
Bi-lobed nucleus
Have large granules containing toxic proteins (can lead to tissue damage)

18
Q

Structure of mast cells?

A

Present in tissue
Single-lobe nucleus, also granulated
IgE receptors on surface
Crosslinking of IgE by allergen causes release of mediators:
- Pre-formed histamines, cytokines, toxic proteins
- Newly synthesized prostaglandins, leukotrienes

19
Q

What kind of allergic diseases are neutrophils important in? Describe their structure.

A

Important in SEVERE or VIRUS-INDUCED ASTHMA + ATOPIC ECZEMA

Multi-lobed nucleus
Granules containing digestive enzymes
Synthesise oxidant radicals, cytokines, leukotrienes

20
Q

Pathogenesis of Acute inflammation in asthma

A

ACUTE Inflammation of airways due to:
MAST cell activation/degranulation

Release of pre-stored (histamine) and newly synthesized (prostaglandins, leukotrienes) mediators

Vascular leakage -> Airway wall oedema
Mucus secretions
SM contraction

TWO phase response - acute early response + late response (hrs later, lesser narrowing)

21
Q

Pathogenesis of Chronic inflammation in asthma

A 
Chronic inflammation due to:
Dense cellular infiltrate (Th2, eosinophils)
Smooth muscle hypertrophy
Mucus plugging
Epithelial shedding
Sub-epithelial fibrosis
22
Q

List important clinical features of asthma

A
  • Reversible generalised airway obstruction
  • Chronic episodic wheeze
  • Bronchial hyperresponsiveness (irritability)
  • Cough
  • Mucus production
  • Breathlessness, chest tightness
  • Reduced/variable Peak flow (PEF)
23
Q

Give Clinical features of allergic rhinitis?

A

Seasonal (hay fever) or Perennial (pets)

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

24
Q

Clinical features of allergic eczema?

A

Chronic itchy skin rash
Usually at flexures of arms/legs
Caused by House dust mite sensitisation, dry cracked skin
Can be complicated by bacterial/viral infections
50% clears by 7 years
90% clears by adulthood

25
Q

Clinical features of anaphylaxis?

A

Severe generalised allergic reaction
Due to generalised degranulation of IgE sensitised mast cells

Symptoms:
Itchiness around mouth/lips
Swelling (lips,throat, other body parts)
Wheeze, chest tightness, dyspnoea
Faintness/collapse
Diarrhoea/vomiting
DEATH if severe/untreated

Potential Systems affected: CVS (collapse), resp (bronchospasm), Skin (vasodilation, redness, angioedema), GI (vomiting/diarrhoea)

26
Q

Investigation of allergies?

A 
Careful history
Skin prick test
RAST (test for IgE in blood)
Total IgE
Lung function (for asthma)
27
Q

Treatment and prevention of anaphylaxis?

A

EpiPen + anaphylaxis kit - antihistamines, adrenaline, streoids

Prevention:
Avoid allergen
Always carry epipen & kit

28
Q

Treatment of rhinitis?

A

Anti-histamines
Nasal steroid spray (for nasal blockage)
Cromoglycate (children, eyes)

If severe: anti-IgE monoclonal antibodies

29
Q

Treatment of eczema?

A

Emollients (keeps skin moist)

Topical steroid cream

30
Q

Treatment of asthma?

A
  1. For mild/intermittent asthma use Short-acting b2 agonist drugs by inhalation (Salbutamol)
  2. Inhaled steroid (low/moderate dose) e.g. Budesonide, fluticasone
  3. Add long-acting bronchodilators/leukotriene antagonist
    HIGH dose inhaled steroids
  4. Add Prednisolone (oral) daily for 7-14 days
    Add anti-IgE, anti-IL-5, anti-IL-4/13 monoclonal Abs
31
Q

Immunotherapy for allergy?

A

Effective for single antigen hypersensitivity
Starting with Injections of low does of purified allergen
Gradually building up to high dose over time
Develops TOLERANCE to allergen

Subcutaneous immunotherapy (SCIT)
or
Sublingual immunotherapy (tablet) (SLIT)
Both therapies need 3 years

Immuno (5 decks)

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