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immunology year 2 > hypersensitivity and allergy > Flashcards

hypersensitivity and allergy Flashcards

1
Q

describe the appropriate immune response

A

they occur to foreign, harmful agents eg viruses, bacteria, fungi and parasites

they are required to eliminate pathogens

there may be tissue damage as a side effect, but as long as the pathogen is eliminated quickly and effectively, the damage will be minimal and repaired easily

involved ag recognition and ab production

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2
Q

examples of things that there is an appropriate immune tolerance to *

A

to self and foreign harmless proteins eg food, pollens, other plant proteins, animal proteins, commensal bacteria

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3
Q

summarise what is involved in appropriate immune tolerance *

A

involves ag recognition and generation of regulatory T cells, rather than reactive ones, and regulatory (blocking) Ab production - IgG4

IgG4 blocks reactibe Ab

ag recognition with danger signals (microbial sequences) leads to immune reactivity

absence of danger = tolerance

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4
Q

what is a hypersensitivity reaction *

A

when an immune response is mounted against:

Harmless foreign ag - in allergy/contact hypersensitivity

autoag - autoimmune disease

alloag - serum sickness, transfusion reactions, graft rejection - ie against benign proteins

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5
Q

how do you classify hypersensitivity reactions *

A

4 types

type 1 - immediate hypersensitivity

type 2 - Ab dependant cytotoxicity

type 3 - immune complex mediated

type 4 - delayed cell mediated

many diseases are a mixture of the types

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6
Q

conditions with type 1 hypersensitivity *

A

anaphylaxis

asthma

rhinitis - seasonal eg for pollen, or perennial for pet or house dust mite (HDM)

food allergy

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7
Q

describe type 1 hypersensitivity *

A

have primary ag exposure

  • leads to sensitisation not tolerance
  • leads to IgE production
  • IgE binds to IgE receptor on mast cells and basophils

have 2nd ag exposure

  • more IgE Ab is produced
  • Ag cross-links IgE on mast cells/basophils - activates intracellular signalling
  • causes degranulation - releases inflammatory mediators
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8
Q

examples and presentations of conditions with type 2 hypersensitivity *

A

clinical presentation depends on the target tissue

organ specific autoimmune

  • myasthenia gravis - anti-ACh receptor Ab - causes muscle weakness
  • glomerulonephritis - anti-glomerular BM Ab - kidney failure from inflammation in glomerulus
  • pemphigus vulgaris - anti-epi cell cement protein ab - causes skin disorder, cement protein hoins the epithelial cells together
  • pernicious anaemia - IF blocking Abs - block absorption of B12

autoimmune cytopenias

  • haemolytic anaemia - RBC
  • thrombocytopenia - platelet
  • neutropenia - WBC
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9
Q

how can you test for Ab dependant hypersensitivity - type 2 *

A

test for specific autoAb

by immunoflurescence or ELISA eg anti-CCP (cyclic citrullinated peptide Abs for rheumatoid arthritis)

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10
Q

describe type 3 hypersensitivity *

A

formation of Ag-Ab complexes in blood

the complex deposits in bv/tissue

this leads to complement and cell activation nad inflammation (inflammatory cells - monocytes and neutrophils)

this leads to activation of other cascades eg clotting

causing tissue damage (vasculitis)

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11
Q

diseases wiuth type 3 hypersensitivity *

A

systemic lupus erythromatosus (SLE) - affect many organs eg kidney = renal failure

vasculatides (poly arteritis nodosum, many different types)

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12
Q

presentations of type 3 hypersensitivity *

A

inflammation of joints, skin (vasculitic rash), gloimerulonephritis, lung

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13
Q

conditions where you get type 4 hypersensitivity *

A

Th1 mediated

  • chronic graft rejection
  • CVHD
  • coeliac disease
  • contact hypersensitivity
  • autoimmune diseases

Th2 mediated - allergic disorders

  • asthma
  • eczema
  • rhinitis
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14
Q

summarise type 4 hypersensitivity *

A

3 main varieties - Th1, cytotoxic, Th2

in Th1

  • transient or persistant ag lead to T cell activation of macrophages or cytotoxic T cells
  • most of tissue damage is dependant on TNF and CTLs

Th2 produce IL4 5 13

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15
Q

describe the mechanism of Th1 mediated responses *

A

ag is taken up by APC

this activates Th1 - Th1 makes INF-gamma - this activates macrophages - macrophages make inflammatory cytokines eg TNF

TH1 also makes IL2 - activates CTLs - CTLs make perforin that kills cells that express the ag

Th1 also make FGF when the reaction is chronic - activates fibroblasts - causes angiogenesis and fibrosis

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16
Q

describe contact hypersensitivity *

A

eg to nickle

immune response when skin is in contact with the ag

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17
Q

summarise the different types of hypersensitivity rn - immune reactant, ag, effector mechanism and example *

A
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18
Q

what is common in all the hypersensitivity reactions *

A

inflammation

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19
Q

describe inflammation *

A

as a result of immune cell recruitment to sites of injury/infection and activation of the immune cells

this leads to production of inflammatroy mediators - complement and cytokines etc

features of inf

  • vasodilation - increased blood flow at site of injury
  • increased vascular permeability - swelling at site of injury
  • inflamm mediators and cytokuines
  • inflamm cells and tissue damage

signs - red, swollen, pain, heat

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20
Q

what causes inreased permeability in inflammation *

A

caused by complement cascade - C3a, C5a, histamine and leukotrienes

21
Q

what are the inflammatory cytokines and chemokines *

A

cytokines - IL1 2 6 TNF INF gamma

chemokines - IL8/CXCL8 (recruit and activate neutrophils), IL10/CXCL10 (recruit and activate lymphocytes)

22
Q

processes involved in inflammatory cell infiltrate *

A

cell traffiking - chemotaxis

cells involved - neutrophils, macrophages, lymphocytes

in Th2 - mast cells and basophils

cell activation

23
Q

what are common allergens

A

pollen

cats

HDM

spores

24
Q

summarise allergy

A

common

severity varies - mild occaisional symptoms, severe chronic asthma, life threatening anaphylaxis

risk factors - genetic and environmental

25
describe the genetic factors that contribute to allergy \*
80% atopies have a FH polygenic - 50-100 genes linked to asthma/atopy genes of IL4 gene cluster (chromosome 5 - IL4 5 13) - linked to increased IgE, asthma and atopy genes on chromosome 11q - IgE receptor linked to atopy and asthma genes linked to structural cells eg epi, linked to eczema (filaggrin gene - expressed in skin and causes cells to adhere) and asthma (Il33, ORMDL3, CDHR3 - all epithelial genes)
26
what are the environmental risk factors for allergy \*
age - increases from infancy, peaks in teens and reduces in adulthood gender - asthma more common in males in childhood and females after puberty - sex hormones important family size - more common in small families and 1st child - less exposure ot pathogens infection - early life infections protect from allergy animals - early exposure protects diet - breast feeding, anti-oxidants and fatty acids protect there is an increase in prevalence of allergy and this is due to environment changes
27
what are the types of inflammation in allergy &
anaphylaxis, urticaria, angioedema - type 1 hypersensitivity (IgE mediated) idiopathic/chronic urticaria (development of itchy wheels and flares) - type 2 (IgG mediated) azthma, rhinitis, eczema - mixed type 1 and 4 (4 is chronic inflammation - cellular inflammatory response)
28
what is necessary for a hypersensitivity reaction \*
development of sensitisation to allergy rather than tolerance - primary response, early in life further allergen exposure to produce disease - memory response
29
describe the mechanism of sensitisation in atopic airway disease \*
allergen arrives and is processedby DC DC presents it to CD4+ niave T cell - thios differentiates into either Th2, Treg or Th1 Treg provides tolerance Th2 is the dominant type in sensitisation Th2 produces IL4 and 13 = proliferation and differentiation of B cells into plasma cells plasma cells do IgE synthesis and release - specific to the ag you have inhaled
30
describe the process that occurs in subsequent exposure to ag \*
allergen arrives at epi processed by DC activates Th2 memory cells cause recruitment and activation of eosinophils eosinophils release IL5, mediators of inflammation are released from eosinophils, mast cells and T cells Th2 memory cells also produce IL4 andd 13 - causing activation of plasma cells and release of IgE
31
describe eosinophils \*
0-5% of blood leukocytes present in blood **recruited during allergic inflammation** generated from bone marrow bilobed nucleus **contain large granules - toxic proteins - degranulation leads to tissue damage** **therapies block activation and recruitment of eosinophils**
32
descibe mast cells \*
tissue residant cells IgE receptors on the surface - bind IgE cross linking of IgE by Ag leads to mediator release the mediators can be preformed in granules - histamine, cytokines or toxic proteins; or newly sythesised - leukotrienes, prostaglandins important in anaphylaxis and urticria
33
describe neutrophils \*
important in virus induced asthma, sever asthma and ectopic asthma (chronic) 55-70% of blood leukocytes polymorphonuclear cells - nucleus contains several lobes granules contain digestive enymes when activated synthesise oxidant radicals, cytokines, leukotrienes
34
describe the immunopathogenesis of asthma \*
acute inflammation of the airways * mast cell activation and degranulation - pre-formed and newly synthesised mediators * this leads to acute airway narrowing - vascular leakage causes airway oedema, mucus secretion blocks airway and sm contraction narrows airway chronic inflammation of the airway * cellular infiltrate of Th2 and eosinophils * leads to sm hypertrophy, mucus plugging, epi shedding and sub epi fibrosis (as result of long term inflammation)
35
important clinical features of asthma \*
reversible generalised airway obstruction - chronic episodic wheeze bronchial hyperresponsiveness - leads to bronchial instability, leads to cough, mucus production, breathlessness and chest tightness there is response to treatment, spontaneous variation and reduced and variable peak flow (PEF)
36
describe the 2 phase response to an allergen \*
quickly get an immediate response - Type 1 hypersensitivity reaction = immediate reduction in lung function - causes prostaglandin and leukotriene release get a later response - further narrowing - cellular response with eosinophils, dc, neutrophils and T cells, macrophages
37
what is the normal PEF (peak flow) for someone with asthma \*
less than 100% - airway obstruction
38
describe a typical day for someone with poorly controlled asthma \*
wheezy on waking took reliever inhaler felt fine ran - exercise induced constriction of the airway have spontaneous reductions because of allergen eposure
39
characteristics of allergic rhinitis \*
seasonal - heyfever, grass, tree pollens perennial allergic rhinitis - HDM, pets sneezing, rhinorrhoea (runny nose), itchy nose and eyes, nasal blockage when chronic - sinusitis and loss of smell/taste, nasal polyp
40
characteristics of allergic eczema \*
chronic itchy rash on skin - in flexures of arms and legs eg behind the knee HDM sensitisation and dry cracked skin = allow penetration of allergen into skin complicated by bacterial and viral infections - early childhood, herpes simplex 50% clears by 7yrs 90% by adulthood
41
describe food allergy \*
infancy - 3yrs - eggs and cow milk children/adults - peanuts, nuts, shell fish, fruits, cereals, soya mild - itchy lips, mouth, angiodema, uricaria - itchy swollen skin rash severe - nausea, abdo pain, diarrhoea, collapse, wheeze, anaphylaxis - low BP and vascular leakage
42
describe anaphylaxis \*
severe generalised allergic reaction uncommon - potentially fatal generalised degranulation of IgE sensitised mast cells symptoms * itchiness around mouth, pharynx, lips * swelling of lips, throat and other parts of body * wheeze, tightness of chest, dysopnoea * faintness, collapse * diarrhoea and vomiting - because of GI oedema and vascular leakage * death is severe and untreated
43
systems involved in anaphylaxis \*
CVS - vasodilation and CV collapse resp - bhronocspasm, laryngeal oedema, and tracheal oedema skin - vasodilation, erythema, urticaria, angioodema GI - vomiting and diarrhoea
44
investigations and diagnosis for allergy \*
careful history skin prick testing - have positive control that gives flare wheel (histamine) and negative control (saline) and see what allergens produce a similar flare wheel RAST test - radioallergosorbant test - put allergen on mem in lab - put blood on mem - if ige to allergen - ige will bind - then add ab to ige with detecting protein attached total IgE in serum - measure of allergy lung function for asthma - peak flow
45
treatment of anaphylaxis \*
emergancy treatment - EpiPen and anaphylaxis kit - antihistamine, steroid, adrenaline, seek immediate medical aid prevention - avoidance of known allergen, carry kit and pen, inform immediate family and care givers, wear a medic alert bracelet
46
treatment of allergic rhinitis \*
anti-histamines for seasonal - sneeze, itch, rhinorrhoea nasal steroid spray - nasal blockage - chronic cromoglycate - children and eyes - blocks degranulation of mast cells
47
treatment of eczema \*
emollients - stop penetration of allergen by improving barrier topical steroid cream - damp down type 4 response in chronic if severe - anti-IgE, anti-IL4/13 (block receptors), anti-IL5 (block recruitment of eosinophils) monoclonal ab
48
describe astham treatment \*
step 1 - short acting B2 agonist - salbutamol or ventolin for mild and intermittent asthma - treat wheeze when it occurs step 2 - inhaled steroid at low-moderate dose - beclomathasone/budesonide or fluticasone - suppress inflammation and prevent asthma step 3 - add long acting bronchodilators, leukotriene antagonist, high dose inhaled steroids step 4 - add courses of oral steroids - SLIT (sublingual immunotherapy) - azithromycin (AB that is anti-viral and anti-inflammatory), prednisolone, anti-IgE, anti-IL5, anti-IL4/13 monoclonal abs
49
describe immunotherapy \*
effective for single ag hypersensitivities eg venom allergy - bee/wasp, pollen, HDM, ag used is purified can have subcutaneous - SCIT - 3yrs - weekly then monthy incjections - need 2hr clinic because need to stay to make sure dont have a serious response SLIT - can be taken at home, safer - 3yrs teach the immune system to be tolerant

immunology year 2 (5 decks)

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