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End Of Year > Immunology > Flashcards

Immunology Flashcards

0
Q

Types of hypersensitivity reactions

A

1- immediate IgE (anaphylaxis)
2- cytotoxic
3- immune complex
4- T cell mediated

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1
Q

Definition of autoimmunity

A
  • influx of auroreactive immune cells and antibodies in body tissues
  • initiates inflammation
  • represents failure of tolerance induction
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2
Q

Types of immune tolerance

A
  • central tolerance
  • peripheral tolerance
    • immune privileged sites
    • anergy/clonal deletion
    • regulatory T cells
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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
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4
Q

Aschoff nodules

A
  • granulomatous inflammation in the myocardium

- centred in interstitium around vessels

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5
Q

Grave’s disease

A
  • anti-TSH receptor antibodies stimulate the production of thyroid hormones
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6
Q

Myasthenia gravis

A
  • anti-ACh antibodies prevent muscles from responding to neuronal impulses
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7
Q

Definition of hypersensitivity

A
  • interaction between the antigen with antibody that is associated with tissue damage/harm
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8
Q

Definition of atopy

A

A familial tendency to develop allergen specific IgE on exposure to environmental allergens and to suffer symptoms

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9
Q

Preformed IgE mediators

A

Histamine

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10
Q

Secondary IgE mediators

A

Prostaglandins and leukotrienes

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11
Q

Management if type 1 hypersensitivity

A
  • avoid allergens
  • stabilize mast cells
  • block mediators (antihistamine)
  • reverse effects of mediators (bronchodilator)
  • immunotherapy
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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
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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
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14
Q

Allergens

A

Antigens which bind IgE

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15
Q

Major allergen of house dustmites

A

Der-p-1

- cysteine protease derived from the gut of the mite

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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
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17
Q

Alternatives to latex gloves

A
  • vinyl

- neoprene

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18
Q

Results of histamine

A
  • rhinorrhoea
  • sneezing
  • increased gastric motility
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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)
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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
Q

Mode of action of type 1 HS

A
  • IgE binds mast cells and basophils with high affinity
  • degranulates
  • releases preformed and secondary mediators
  • local inflam or generalized effects
25
Q

Physiological role of type 1 HS

A

Parasite elimination

26
Q

Mode of action of type 2 HS

A
  • antibodies of IgG, IgA or IgM combine ith antigen on surface of cell or basement membrane
  • activate complement or lymphocytes
27
Q

Physiological role of type 2 HS

A

Pathogen lysis

28
Q

Management of type 2 HS

A
  • steroid therapy
  • plasmapheresis (good pastures)
  • exchange transfusion (Rh incom)
29
Q

Physiological role of type 3 HS

A

Transport of antigens to germinal centres

30
Q

How to detect type 3 HS

A

Clq binding assay

31
Q

Treatment of type 3 HS

A
  • corticosteroids

- elimination of antigen

32
Q

Management of type 4 HS

A
  • treat underlying infection

- steroids to suppress inflam

33
Q

List allergenic trees

A
  • oak
  • plane
  • willow
  • cypress
  • eucalyptus
  • birch
34
Q

Define desensitization

A

Rapid state of tolerance achieved by injecting multiple increasing doses of antigen to patients in ICU

35
Q

Define immunotherapy

A

Gradual state of tolerance achieved over months to unavoidable environmental allergens by repeated subcutaneous injections or exposure to allergen under the tongue

36
Q

Mechanism of immunotherapy

A
  • 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
Q

Allergic cytokines

A

IL3 - mast cell maturation
IL4 - IgE produced
IL5 - eosinophil differentiation

38
Q

Requirements before starting immunotherapy

A
  • IgE mediated sensitivity has major relevance in symptoms and severity
  • allergen is unavoidable
  • single allergen responsible
39
Q

When is immunotherapy used for patients with pollen or mite allergy

A

When non sedating antihistamines and topical therapy do not relieve symptoms

40
Q

Contraindications of immunotherapy

A
  • extracts of unproven efficacy
  • infancy or old age
  • pregnancy
  • severe atopic dermatitis
  • diseases with contraindication for use of epinephrine
  • uncontrolled asthma
41
Q

How T cells provide protective immunity against mycobacteria

A
  • CD4 cells release IFN-y to activate macs to kills ingested organisms
  • CD8 cells kill infected cells
42
Q

How mycobacteria survive in macs

A
  • inhibit phagolysosomal fusion
  • secrete anti-oxidants to neutralize ROS
  • kill macs by inducing membrane rupture
43
Q

How cytotoxic T cells kill cells

A
  • by cytotoxic granules (perforin pores)

- by Fas/FAS L proteins

44
Q

Causes of reactivation of TB

A
  • malnourishment and alcohol
  • diabetes
  • steroid therapy
  • immunosuppressive and cytotoxic agents
  • HIV
  • vit D deficiency
45
Q

Local effects of TNF

A
  • increased granuloma formation
  • increased microbial killing
  • monocytes activation
46
Q

Systemic effects of TNF

A
  • fever
  • weight loss
  • necrosis
47
Q

Explain the relationship between vitamin D and TB

A
  • 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
Q

Cathelicidin antibacterial activity mediated by

A
  • direct killing of MTB
  • production of ROS
  • overcoming the inhibition of phagolysosomal fusion
49
Q

3 molecules in macs that can kill MTB

A
  • NO
  • granulysin
  • cathelicidin
50
Q

Causes of negative Mantoux test

A
  • early stage TB infection
  • never exposed
  • anergy due to systemic disease
  • anergy due to sever TB
51
Q

Why does BCG offer limited TB protection

A
  • protection varies widely in different pops
  • limited extent of protection
  • limited duration of protection

End Of Year (12 decks)

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