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Year 2 : MCD > Immunology 3: Hypersensitivity and allergy > Flashcards

Immunology 3: Hypersensitivity and allergy Flashcards

1
Q

What are appriate immune reaction?

A

Response to foreign harmful argents such as virus, bacteria, fungi, parasites
Eliminate pathogens
Can cause tissue damage as a side effect but if the patogen is elminated then can be repaired
Involves Ag recognition by immunesystem

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2
Q

What is appropriate immune tolerance?

A

Tolerance to self Ag, and foreign Ag that cause no harm-food, pollen, plant proteinsm animal, commensals bacterua
Involves Ag recognition and Treg and regulatory blocking IgG4 AB
antigen in context of danger (microbial signals) cause immune response, and absence of danger-tolerance (unsure how)

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3
Q

When do hypersensitivity responses happen?

A

When react to harmless foreign Ag-allergy
Autoantigens-AID
alloantigens-foreign from human-serum sickness, tranplsant,

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4
Q

What are the 4 types of hypersensitivty reaction?

A

Type 1-immeduate
II-Ab dependent
III-immune complex
IV-delayed cell

these are distincts but most disease involve more than one

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5
Q

When is type 1 hypersensitivity important?

A

Anaphylaxis, ashtma, rhinitis-seasonal and perennial

food allergy

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6
Q

How does type 1 hypersensitivity develop?

A

1st AG exposure-inital
Sensitisation and not tolerance
IgE production in response-IgE bind mast cells and basophils

2nd Ag exposure-more IgE produce
Ag cross link IgE on mast cell/baso-degranulation

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7
Q

What is type II hypersensitivity and how does it present? How do you test?

A

Depends of Ab against the AG
depends on which organ affected-mysternia gravis wiith Anti acetycholin AB, glomerulonephritis-glomerual BM
Pemphigus vulgaris-blistering of skin
Pernicious aneamia

OR Autoimmune cytopenias-AB mediated blood cell destruction
Heamolytic aneamia, thrombocytopenia, neutropenia

test by testing for specific AB=with immunofluorescnence and histology, or ELISA test

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8
Q

What is Type III hypersensitivity? What is made from?

A

Formation of Ag -Ab complexes
COmplex deposite in smaller vessels-complement and cell activation (monocytes, neutrophils), activation of cascades (clotting)-Tissue damage (kidneym skin, lungs
common in SLE, Vasculidities

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9
Q

What is type IV hypersensitivity? what mediated by? Main pathways?

A

delayed-cell mediated
Chronic graft rejection, graft vs host, coeliac, contact hyper, AID –th1 mediated
ashtma, thinitis, eczema-th2 mediated

Th1-produce INFgamma, cytotoxic cells, and th2
transiet/persitant Ag-activation of T cells+macrophages-CTL
Tissue damage dependent on TNF and CTL (th1 produce IL2 to activation of CTL) or IFNgamma to macrophage to make TNF
also activtion of fibroblast

typical in metal reaction-contact hypersensitivity

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10
Q

What is the role of inflammation in hypersensitivity?

A

present in all types-
Reaction of recruitment and activation of cells to site of injuery
Mediated by cytokines

cause vasodilation-complement (C3, histamine), vascular permeability, increase in mediator and cytokines (Il1, 6, 2, TNF, INFy), chemotaxis cytokine-IL* (neutrophils), IP 10 (lymphocytes)
inflam cells and tissue damage
cause 4ors-redness, heat, damage, pain

involve neutrophils, macrophagesm lymphocytes and mast cells

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11
Q

How common is allergy?

A

Atopy-50% in UK
severity varies-midl symtoms, severe chronic ashtma, anaphylaxis
risk factors are genetic and environemental

increasing prevalence in UK-from 4% in 69 to 20% in 2009-probably environemental

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12
Q

What is the role of genetics in allergy?

A

important-80% that have allergy have family history
but polygenic-100 identified
important-genes in IL4 cluster-raised IgE, asmta and atropy
IgE receptor genes-allergy and ashtma
Genes to structural cells linked to eczema (like filagrin

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13
Q

What is the role of environement in Allergy

A

Imporntant-increase with age-peak in teenage years
Gender-more common in males in childhood, adult-female
Family size-more common in small families (lots of other to exposure them)
Infection-early infections protect
Animals-early exposure protects
diet-breast feeding, antioxidants, fatty acid protect

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14
Q

What are the 3 types of inflammation in allergy>

A

Most common-anaphylaxis, urtucariam angioodemia-Type 1
Idiopathuc.chronic urticarua-type II
Ashma, rhinitis, eczema-mix of type 1 and type IV

Always requires sensitisation and then further exposure produce the response

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15
Q

Describe classical pathogenesis of allergy in lungs

A

Antigen taken up by DC-process into peptide and present to local T helper cells-either become Th1 , Treg or Th2-when sensitise instead of tolerate-Th2
Produce IL4/13–b cells then produce IgE-proliferate and differentiate–produce IgE to Ag

when Ag again-memory T cells from before produce more Il4/13-produce more IgE-and IL5, recruiting eosinophils-inflammation
Also mast cells and basophils

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16
Q

Which cells are the most important in allergy?

A

eosinohphils-low in blood but high in tissue-recruited in allergy-bilobbed nucleus + granules-toxic proteins-leads to tissue damage-very in asthma

mast cells-immediate/anaphylaxis-resident in tissue-IgE receptor-Cross linking of IgE on large Ag-mediator release of granules (histamine, cytokines, toxic proteins) and newly synthesises-leukotrienes, prostagrlandins

neutrophils-virus induces asthma attacts, crhonic eczema-common in blood-polymophonuclear cells-granules have digestive enzymes and synthesis ROS, Cytokine and leukotrienes

17
Q

Describe the immonopathogensis of asthma>

A

Actue inflam of airway
Mast cell activation and degranulation-histamine, prostaglanding, leukotriens => acute narrowing (consquence of vascular leakage-swelling of tissue
lead to mucus secretion and filling of airway
and SMC constriction, all combined block airway

2 phase response-large, peak response immediate (early response-leukotriene, histamine), then 6h-smaller but longer resonse–consquence of cellular response-eosinohils, macrophages, neutrophils

18
Q

Describe the chronic inflammations of airway in asthma?

A

Cellular infiltrates-SMC hypertrophy, mucus pluggingm epithelial shedding and sub epithalial fibrosis

19
Q

What are the clinical features of asthma>

A

Revesribke generilsed aiway obstructuion-chronic episodic wheezze
bronchial hyperresponsitivity
Cough, mucus production
breathlessness, chest tightness

important-response to treatment, spontaneous variation and reduce/variable PEF –varies a LOT during day

20
Q

What is allrergic rhinits?

A

seasonal-hayfeaverl, etc
Perinial-all year0pets
sneezing, rhinorrhoae, itchy nose, eyes
Nasal block, sinusitis, loss of smell taste, nasal polyps

21
Q

What are features of allergic aczema-

A

Chronic itchy skin rash-usually at flexture of arm and legs
sensitisation and dry cracked skin
complicated rarely by infection

but usually clears away from small children -90% lose it by adulthood

22
Q

What is food allergy?

A

infancy-eggs, milk
Adults-peanutsm shellfish, fruits, cereal, soya

mild-itchy lips, mouth, angiodeamiam urticaria
severe-nausea, abdopain, collapse, wheeze, anaphalaxics

23
Q

What is anaphylaxis? How do treat it?

A

severe generalise reaction-uncommon
fatal–generalised degranulation of IGE sensitised mast cells
Cause itchy mouth lipds, mouth, parynx (swelling_
wheeze, dysnpnea, faitness, collapse, DnV
vasodilation, cardio collapse, bronchospasm, larygeal odema, vasodilation of skin, utricaria, angioodeamia, DnV

treat with epipen-adrenaline-
a kit-also antihistamines, steroids–rest is medical aid

Main in prevent-avoid allergen, carry epipen, inform people around u

24
Q

What are the main diagnostic test for allergy?

A 
careful hisotyr is main one
Skin prick test
RAST-blood specific IgE test
Total IgE
Lung function for ashtma
25
Q

What is the main treatment for rhinitis and eczema>

A

If mild-antihistamines will do
steroid spray-for nasal blockage
Cromoglyctae (children eyes)-block degranulation of mast cells

eczema-emoliants-improve skin barrier, topical steroid cream

If severe-Anti IgE, AntiIl4, anti IL5, anti IgE mAB

26
Q

What are the main treatment for asthma

A

B2 agonist-Salbutamol
Inhaled steroids-becolmethasone/budesonide
more=long acting bronchodilators(leukotriens antagonsit), more steroids
Oral steroids, immune therapy, arithromycin (Abx also anti inflam, and mAb vs IL4/5)
Immunotherapy-effective for single Ag hypersensitivty-

27
Q

What is immunotheraoy for allergy>

A

Immunotherapy-effective for single Ag hypersensitivty-venoms, pollens, mites,
need subcutaneous immunitherapy-3 years to form reduce sensitivity-weekly/monthly-stay for 2h visits in case of response
Sublingual-can be taken at home for 3 years-doesnt cause massive response

teaches immune system tolerance

Year 2 : MCD (38 decks)

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