Immunology Flashcards
0
Q
Types of hypersensitivity reactions
A
1- immediate IgE (anaphylaxis)
2- cytotoxic
3- immune complex
4- T cell mediated
1
Q
Definition of autoimmunity
A
- influx of auroreactive immune cells and antibodies in body tissues
- initiates inflammation
- represents failure of tolerance induction
2
Q
Types of immune tolerance
A
- central tolerance
- peripheral tolerance
- immune privileged sites
- anergy/clonal deletion
- regulatory T cells
3
Q
Mechanisms of loss of self tolerance
A
- loss of immunological privileged status (infection)
- viral/drug induced altered self AG (hemolytic anaemia)
- regulatory T cell dysfunction
- molecular mimicry
4
Q
Aschoff nodules
A
- granulomatous inflammation in the myocardium
- centred in interstitium around vessels
5
Q
Grave’s disease
A
- anti-TSH receptor antibodies stimulate the production of thyroid hormones
6
Q
Myasthenia gravis
A
- anti-ACh antibodies prevent muscles from responding to neuronal impulses
7
Q
Definition of hypersensitivity
A
- interaction between the antigen with antibody that is associated with tissue damage/harm
8
Q
Definition of atopy
A
A familial tendency to develop allergen specific IgE on exposure to environmental allergens and to suffer symptoms
9
Q
Preformed IgE mediators
A
Histamine
10
Q
Secondary IgE mediators
A
Prostaglandins and leukotrienes
11
Q
Management if type 1 hypersensitivity
A
- avoid allergens
- stabilize mast cells
- block mediators (antihistamine)
- reverse effects of mediators (bronchodilator)
- immunotherapy
12
Q
Pathogenesis of type 3 hypersensitivity
A
- union of antigens and antibodies to form insol immune complexes
- fix in sites and activate complement
- release anaphylotoxins
- release mast cell mediators
- influx of leukocytes
- phagocytose complement
- damage local tissue
- intensify inflammation
13
Q
Pathogenesis of type 4 hypersensitivity
A
- perivascular cuffing of inflam cells
- polys migrate out of lesion (mononuclear cell infiltrate)
- exaggerated reaction between antigen and helper cell
- release cytokines which attract macs and help cytotoxic T cells to become killer cells
- cause tissue damage
14
Q
Allergens
A
Antigens which bind IgE
15
Q
Major allergen of house dustmites
A
Der-p-1
- cysteine protease derived from the gut of the mite
16
Q
Components of bee venom
A
Vasoactive amines - histamine - dopamine - noradrenaline Peptides - apamin - melitin - mast cell degranulating peptide Enzymes - phospholipase A - hyaluronidase - acid phosphatase
17
Q
Alternatives to latex gloves
A
- vinyl
- neoprene
18
Q
Results of histamine
A
- rhinorrhoea
- sneezing
- increased gastric motility
19
Q
Results of activation of complement system that is important in immune defence against bacteria
A
- opsonisation (enhanced uptake by phagocytosis)
- formation of MAC (damage to bacterial membr leading to osmotic lysis)
- triggering of acute inflam response (anaphylotoxins C3a and C5a increase vessel perm)
20
Q
1st antibodies to be made after exposure
A
IgM
21
Q
2nd antibodies made after exposure
A
IgG
22
Q
How secondary antibody response differs from primary antibody response
A
- upon re-encounter with antigen, secondary antibody response is IgG, high titre, faster and has better fit to antigen
23
Q
Describe opsonisation
A
Coating of pathogen with antibodies/complement fragments that facilitates phagocytosis by phagocytes (macs)
24
Mode of action of type 1 HS
- IgE binds mast cells and basophils with high affinity
- degranulates
- releases preformed and secondary mediators
- local inflam or generalized effects
25
Physiological role of type 1 HS
Parasite elimination
26
Mode of action of type 2 HS
- antibodies of IgG, IgA or IgM combine ith antigen on surface of cell or basement membrane
- activate complement or lymphocytes
27
Physiological role of type 2 HS
Pathogen lysis
28
Management of type 2 HS
- steroid therapy
- plasmapheresis (good pastures)
- exchange transfusion (Rh incom)
29
Physiological role of type 3 HS
Transport of antigens to germinal centres
30
How to detect type 3 HS
Clq binding assay
31
Treatment of type 3 HS
- corticosteroids
| - elimination of antigen
32
Management of type 4 HS
- treat underlying infection
| - steroids to suppress inflam
33
List allergenic trees
- oak
- plane
- willow
- cypress
- eucalyptus
- birch
34
Define desensitization
Rapid state of tolerance achieved by injecting multiple increasing doses of antigen to patients in ICU
35
Define immunotherapy
Gradual state of tolerance achieved over months to unavoidable environmental allergens by repeated subcutaneous injections or exposure to allergen under the tongue
36
Mechanism of immunotherapy
- specific IgE rises and then declines
- specific IgG rise
Also
- generation of specific T reg cells
- decreased prod of lymphocyte mediators
- reduced wheal and flat response
- increased IgA secretion
37
Allergic cytokines
IL3 - mast cell maturation
IL4 - IgE produced
IL5 - eosinophil differentiation
38
Requirements before starting immunotherapy
- IgE mediated sensitivity has major relevance in symptoms and severity
- allergen is unavoidable
- single allergen responsible
39
When is immunotherapy used for patients with pollen or mite allergy
When non sedating antihistamines and topical therapy do not relieve symptoms
40
Contraindications of immunotherapy
- extracts of unproven efficacy
- infancy or old age
- pregnancy
- severe atopic dermatitis
- diseases with contraindication for use of epinephrine
- uncontrolled asthma
41
How T cells provide protective immunity against mycobacteria
- CD4 cells release IFN-y to activate macs to kills ingested organisms
- CD8 cells kill infected cells
42
How mycobacteria survive in macs
- inhibit phagolysosomal fusion
- secrete anti-oxidants to neutralize ROS
- kill macs by inducing membrane rupture
43
How cytotoxic T cells kill cells
- by cytotoxic granules (perforin pores)
| - by Fas/FAS L proteins
44
Causes of reactivation of TB
- malnourishment and alcohol
- diabetes
- steroid therapy
- immunosuppressive and cytotoxic agents
- HIV
- vit D deficiency
45
Local effects of TNF
- increased granuloma formation
- increased microbial killing
- monocytes activation
46
Systemic effects of TNF
- fever
- weight loss
- necrosis
47
Explain the relationship between vitamin D and TB
- monocytes and neutrophils have defensins and cethelicidin in their granules
- IFN-y activates macrophage 1a-hydroxylase and formation of 1,25 (OH) vit D3
- induces carhelicidin- mediated killing of MTB
- monocytes vit D3 formation is not under negative feedback so systemic spillover rarely occurs
48
Cathelicidin antibacterial activity mediated by
- direct killing of MTB
- production of ROS
- overcoming the inhibition of phagolysosomal fusion
49
3 molecules in macs that can kill MTB
- NO
- granulysin
- cathelicidin
50
Causes of negative Mantoux test
- early stage TB infection
- never exposed
- anergy due to systemic disease
- anergy due to sever TB
51
Why does BCG offer limited TB protection
- protection varies widely in different pops
- limited extent of protection
- limited duration of protection
