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Emily Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

What is innate immunity?

A
  • Instinctive,
  • non-specific,
  • does not depend on lymphocytes,
  • present from birth
  • Cells involved: Neutrophils, macrophage, basophils, eosinophils, mast cells, natural killer cells
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2
Q

What is adaptive immunity?

A
  • Specific,
  • Acquired immunity
  • requires lymphocytes
  • antibodies
  • Cells involved: T helper cells, cytotoxic T cells, B cells
  • quick response on second encounter
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3
Q

What are the 3 modes of action for complement factors?

A
  1. Direct Lysis
  2. Attract more leukocytes to site of infection
  3. Coat invading organism
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4
Q

What are the 5 classes of antibodies?

A

IgG
IgA
IgM
IgD
IgE

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5
Q

What are cytokines? And types?

A

Proteins secreted by immune and non-immune cells

  1. Interferons
  2. Interleukins
  3. Colony stimulating factors
  4. Tumour necrosis factors
  5. Chemokines
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6
Q

What are interferons (IFN)?

A

Induce a state of antiviral resistance in uninfected cells

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7
Q

What are Interleukins (IL)?

A
  • Produced by many cells, over 30 types
  • Can be pro-inflammatory (IL 1) or anti-inflammatory (IL 10)
  • Can cause cells to divide, to differentiate and to secrete factors
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8
Q

What are colony stimulating factors?

A

Involved in directing division and differentiation of bone marrow stem cells
(precursors of leukocytes - drive production of WBCs)

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9
Q

What is the role of tumour necrosis factors?

A

Mediate inflammation and cytotoxic reactions
- pro inflammatory

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10
Q

What is the role of chemokine?

A

Leukocyte chemoattractants
- attract appropriate leukocytes to sites of infection/inflammation
- direct from the blood stream into tissues or lymph organs

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11
Q

What is innate immunity composed of?

A
  • Physical and chemical barriers
  • Phagocytic cells (macrophage and neutrophils)
  • Blood proteins (complement, acute phase)
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12
Q

What are the roles of complement factors?

A

Once activated they can:
1. Lyse microbes directly (Membrane attacking centre MAC)
2. Chemotaxis
3. Opsonisation (enables pathogens to be engulfed more easily)

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13
Q

Why do we need adaptive immunity?

A
  • microbes evade innate immunity
  • intracellular viruses and bacteria ‘hide’ from innate immunity
  • need memory to specific antigen (faster response)
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14
Q

What must the immune system do in order to be effective?

A

The immune system has discriminate self from non-self

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15
Q

Give examples of physical and chemical barriers used in innate immunity?

A

Skin, mucociliary escalator, gastric acid, hairs, lysozymes etc.

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16
Q

How does cell mediated immunity work?

A

interlay between:
- antigen presenting cells
- and T cells

Requires intimate cell to cell contact
- to control Ab responses via contact with B cells
- to directly recognise and kill viral infected cells

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17
Q

What is the major histocompatibility complex (MHC)?

A

A group of genes that code for proteins found on the surfaces of cells that help the immune system recognise foreign substances.
- the 2 ways that antigens are presented on the cell surface

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18
Q

How are antigens presented by MHC1?

A
  1. Endogenous antigens are broken by proteosome into peptides
  2. Peptides delivered into endoplasmic reticulum by a TAP transporter
  3. TAP interacts with MHC1 molecule
  4. MHC1 permanently binds to one of the peptides
  5. TAP transporter and helper proteins dissociate
  6. Antigen loaded MHCI migrates through Golgi apparatus to cell surface
  7. MHCI released onto cell surface to be recognised by CD8 T cells

occurs in all nucleated cells

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19
Q

How are antigens presented by MHCII?

A
  1. Exogenous cells are taken up by cells with endocytic activity
  2. Taken into endosome
  3. MHCII already bound to small molecule
  4. Helper proteins help exchange small molecule for an antigen
  5. Vesicle containing MHCII travels to cell surface
  6. Antigen now recognised by CD4 T helper cells

(Help B cells make antibodies to extracellular pathogen. can help directly kill)

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20
Q

Give 3 functions of antibodies?

A
  1. Neutralsie toxin by binding to it
  2. Increase opsonisation (process by which pathogens are marked for phagocytosis)
  3. Activate complement

Link between innate and adaptive immunity

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21
Q

What is the structure of an antibody?

A
  1. Antigen recognition
    - Fab regions (V of Y shape): variable in sequence
    - bind different antigens specifically

Joined by ‘hinge region’

  1. Antigen elimination
    - Fc region (stem of Y) - constant in sequence
    - Binds to complement
    - Fc receptors on phagocytes
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22
Q

What does variable and constant antibody regions do?

A

Variable
- antigen recognition
- Bind antigen
- differ between antibodies with different specificities

Constant
- determines mechanism used to destroy antigen
- same for antibodies of a given H chain class or L chain type

Constant and variable regions are encoded by separate exons

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23
Q

What is the role of IgG?

A
  • most abundant in BLOOD
  • main class in serum and tissues
  • important in secondary response
  • can cross placenta
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24
Q

What is the role of IgM?

A
  • Important in primary response
  • Mainly found in blood (too big to cross epithelium)
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25
Q

What is the role of IgA?

A
  • In serum & secretions protects mucosal surfaces
  • present in breast milk & neonate gut
  • important in combatting pathogens outside of the body
    (most abundant in total body)
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26
Q

What is the role of IgD?

A
  • not that important
  • a transmembrane monomeric form is present on mature B cells
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27
Q

What is the role of IgE?

A
  • involved in allergy & parasitic infections
  • present at very low levels
  • Basophils and mast cells express an IgE-specific receptor that has high affinity for IgE and triggers release of histamine
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28
Q

What is a haematopoietic pluripotent stem cell?

A

(hemocytoblast)
Stem cells that every blood cell in the body originates from

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29
Q

What are the 3 types of polymorphonuclear leukocytes?

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
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30
Q

What are 3 types of mononuclear leukocytes?

A
  1. Monocytes
  2. t cells
  3. B cells
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31
Q

What is the function of neutrophils?

A
  • Plays an important role in innate immunity (phagocytosis)
  • 2 main intracellular granules
    1. Primary lysosomes - can kill microbes by secreting toxic substances
    2. secondary granules
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32
Q

What is the function of monocytes?

A
  • Plays an important role in innate AND adaptive immunity (phagocytosis and antigen presentation)
  • differentiate in macrophages in the tissues
  • remove anything foreign or dead
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33
Q

What is the function of macrophages?

A
  • importnat in innate & adaptive
  • resides in tissues e.g., kupffer cells, microglia
  • first line of non-self recognition
  • remove foreign and self ( tumour/dead cells)
  • present antigen to T cells
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34
Q

What is the function of eosinophils?

A
  • parasitic infections and allergic reactions
  • lifespan 8-12 days
  • granules stain fo acidic dyes
  • activates neutrophils, induceing histamine release from mast cells
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35
Q

What is the function of basophils?

A
  • parasitic infections and allergic reactions
  • bind to IgE to receptor to release histamine
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36
Q

What is the function of mast cells?

A
  • only in tissues
  • bind to IgE releasing histamine
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37
Q

What are the 4 main types of T cells?

A
  1. T helper cells 1 (CD4) - help immune response to intracellular pathogens
  2. T helper cells 2 (CD4) - help produce antidodies extracellular pathogens
  3. cytotoxic T cell (CD8) - kill cells directly
  4. T regulator - regulate immune responses
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38
Q

Where do T and B cells mature?

A

B cells = bone marrow
T cells = Thymus

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39
Q

What is the function of natural killer cells?

A
  • found in spleen, tissues
  • recognise and kill by apoptosis; virus infected cells & tumour cells (mainly in antiviral and cancer)
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40
Q

What are the 2 types of complement factor pathway initiators?

A
  1. Classical = antibody bound to microbe
  2. Alternative = C binds to microbe
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41
Q

What is the response to a skin barrier being breached?

A
  1. Stop bleeding (coagulation)
  2. Acute inflammation (leukocytes recruitment)
  3. Kill pathogens, neutralise toxins, limit pathogen spread
  4. Clear pathogens/dead cells (phagocytosis)
  5. proliferation of cells to repair damage
  6. Remove blood clot - remodel extracellular matrix
  7. Re-establish normal structure/function of tissue
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42
Q

What are the steps of phagocytosis?

A
  1. Binding
  2. Engulfment
  3. Phagosome formation
  4. Lysosome fusion (phagolysosome)
  5. Membrane disruption
  6. Antigen presentation/secretion
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43
Q

Which cells express MHC1?

A

All nucleated cells express MHC1. e.g. a virus infected or cancer cell would express MHC1.

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44
Q

Which cells express MHC2?

A

Antigen presenting cells ONLY e.g. macrophages, B cells, dendritic cells.

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45
Q

What is the role of MHC 3?

A

Code for secreted proteins

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46
Q

Which MHC would an intracellular antigen (endogenous) lead to the expression of?

A

MHC 1

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47
Q

Which MHC would an extracellular antigen (exogenous) lead to the expression of?

A

MHC 2

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48
Q

Which interleukin is secreted when a helper T cell is bound to a T cell receptor?

A

IL-2.
This then binds to an IL-2 receptor on the T cell and produces a positive feedback mechanism leading to division and differentiation.

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49
Q

Define epitope

A

The part of the antigen that binds to the antibody/receptor binding site

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50
Q

Define affinity

A

Measure of binding strength between an epitope and an antibody binding site. The higher the affinity the better.

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51
Q

Describe the process of a T helper cell binding to a B cell.

A
  1. A B-cell antibody binds to an antigen
  2. phagocytosis
  3. epitope is displayed on the surface of the B-cell bound to an MHC2
  4. TH2 binds to B-cells
  5. cytokine secretion induces B-cell clonal expansion
  6. differentiation into plasma cells and memory B cells.
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52
Q

What are the 3 layers of blood?

A

Upper fluid - plasma
Middle - Buffy coat, WBCs
Lower - erythrocytes, platelets

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53
Q

What is a dendritic cell?

A
  • antigen presenting cell
  • mesenchymal cell origin NOT haematopoetic
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54
Q

What are the physical defences?

A
  • saliva
  • tears, lysozyme in tears and other secretions
  • low Ph and commensals of vagina
  • mucous secretions
  • mucous –> entrapment
  • cilia –> beating removes microbes
  • commensal colonies –> attachment, nutrients
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55
Q

What is PAMP?

A

Pathogen Associated Molecular Patterns

(patterns that are recognised to not be human, these are patterns only pathogens have)

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56
Q

What are PRRs?

A

Pattern Recognition Receptors

(patterns only on pathogens)

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57
Q

What happens to T cells that recognise ‘self’?

A

They are killed in the foetal thymus
- now only recognise ‘non-self’
- only activated when antigen is presented

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58
Q

What is the activation of T cells?

A

Naive T cells
1. split into CD4 (T helper cells) and CD8 (cytotoxic T cells) –> kill intracellular pathogens
2. CD4 split into Th1(helps kill intracellular pathogens) or Th2 (antibody production)

Both types of Th are cytokines

59
Q

What happens to B cells that recognise self?

A

Killed in bone marrow

60
Q

How do we handle bacteria and viruses differently?

A

Bacteria & fungi = phagocytosis and killing

Viruses = cellular shut down, self-sacrifice, cellular resistance

61
Q

What are the 2 types of PRR?

A
  1. secreted and circulating PRR’s
  2. Cell-associated PRR’s (more traditional receptors)
62
Q

How do cell associated PRRs function?

A
  • Receptors that are present on the cell membrane or in the cytoskeleton of the cells
  • recognise a broad range of molecular patterns
  • TLRs (Toll like receptors) are the main family
63
Q

What are TLRs?

A

Toll-like receptors
- class of proteins expressed on macrophages and dendritic cells
- send signals to the nucleus to secrete cytokines and interferons
- these signals initiate tissue repair
- enhanced TLR signalling = improved immune response

64
Q

What are NLRs?

A

Nod-like receptors
- proteins that detect intracellular microbial pathogens
- release cytokines and can cause apoptosis if the cell is infected

65
Q

What are some examples of TLRs?

A

TLR1/2 = gram positive lipopeptides
TLR 4 = used in vaccine adjuvants

66
Q

What are RLRs?

A

RIG-like receptors
- detect intracellular double stranded viral RNA and DNA
- activate interferon production, enabling an antiviral response

67
Q

How do TLRs and PRRs aid in immunity?

A

They drive cytokine production, thus activating antigen presenting cells, that then activate T cells

68
Q

What are the 3 main types of vaccines?

A
  • Whole killed
  • Toxoids
  • Live attenuated
69
Q

What is passive immunity?

A

A short term immunity which results from the introduction of antibodies from another person or animal

70
Q

What are the advantages and disadvantages of passive immunity?

A

Pros:
- gives immediate protection
- effective in immunocompromised patients

Cons:
- Short lived
- Possible transfer of pathogens

71
Q

What is natural and artificial passive immunity?

A

Natural = transfer of maternal antibodies across the placenta to the foetus/breast milk

Artificial = treatment with pooled normal human IgG or immunoserum against pathogen

72
Q

What are the 2 types of non-living vaccines and their limitations?

A
  1. Whole killed vaccines
    - antigens in it induce an immune response
    limitations: organisms grown in vitro, side effects (reactogenicity), need multiple vaccines
  2. Toxoids
    - cell free toxoids (inactivated toxins)
73
Q

How does a live attenuated vaccine work?

A

The organism replicate within the host and induce an immune response
- now protected against the actual organism

74
Q

What are the advantages and disadvantages of live attenuated vaccines?

A

Pros:
- lower doses required, so less needed to be grown
- immune response more closely mimics a real infection
- route of ad ministration may be more favourable
- fewer doses may be required

Cons:
- hard to balance attenuation (weaker version) and immunogenicity (ability to induce immune response)
- cannot be used on immunocompromised
- might reverse to being harmful again

75
Q

Explain the stages of vaccination?

A
  1. Engage the innate immune system (neutrophils, dendritic cells, macrophages)
  2. Elicit danger signals that activate the immune system
    - engage PAMPs and TLRs
  3. activate specialist antigen presenting cells e.g. langerhans
  4. Engage the adaptive immune system
    - generate memory T and B cells
    - activate T helper cells
76
Q

Examples of a whole organism vaccine.

A
  1. Tuberculosis - BCG
  2. Polo Sabin
77
Q

What are 3 types of subunit vaccines?

A

Purified molecular components as immunogenic agents.

  1. Inactivated exotoxins
    - some pathogens produce the symptoms of disease as a result of exotoxins
    - toxoid (heat treated or chemically modified to eliminate toxicity)
  2. Capsular polysaccharides
    - highly polar
    - block opsonisation
  3. Recombinant microbial antigens
78
Q

How do DNA vaccines work?

A
  • transiently express genes from pathogens in host cells
  • generates immune response similar to natural infections
79
Q

How do recombinant vector vaccines work?

A
  • imitate effects of transient infection with pathogen but using a non-pathogenic organism
  • genes for pathogen are put into a non-pathogenic microorganism
80
Q

What are the components of a vaccine?

A
  1. Active ingredients
    - viral or bacterial antigens
  2. Adjuvants
    - stimulate the immune system
  3. antibiotics
    - prevent contamination by bacteria
81
Q

Name 3 receptors that make up the PRR family.

A
  1. Toll Like receptors (TLR)
  2. Nod-like receptors (NLR)
  3. Rig-like receptor (RLR)
82
Q

What disease could be caused by a non-functioning mutation in NOD2?

A

Crohn’s disease

83
Q

Give examples of diseases that can be caused by PRR’s failing to recognise pathogens

A
  1. Atherosclerosis
  2. COPD
  3. Arthritis
84
Q

Give examples of 3 extracellular PRR.

A
  1. Mannose receptors
  2. Scavenger receptors
  3. TLR’s
85
Q

What is the function of mannose and scavenger extracellular receptors?

A

They induce pathogen engulfment.

86
Q

Give an example of an intracellular PRR.

A

NLR

87
Q

What diseases do polysaccharide vaccines treat?

A
  • Pneumococcal disease
  • Salmonella Typhi
  • Meningococcal disease
88
Q

What are 2 features of the adaptive immune response?

A
  1. Unmethylated CpG sequences
  2. Lectin type molecules
89
Q

What are examples of classical PAMPs?

A

Are on micro-organisms and recognised by PRRs

o Flagellin - a protein found in bacterial flagella
o Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria
o Peptidoglycan - found in bacterial cell walls
o Lipoarabinomannan of mycobacteria

90
Q

Which UK vaccines are administered as live attenuated vaccines?

A
  • MMR
  • BCG (TB)
91
Q

What is the type 1 hypersensitivity reaction?

A

Antigen reacts with IgE released from mast cells
e.g. anaphylaxis

92
Q

What is the type 2 hypersensitivity reaction?

A

IgG or IgM binds to antigen on cell surface
e.g. Rheumatic fever

93
Q

What is the type 3 hypersensitivity reaction?

A

Free antigen and antibody combine (IgG/IgM complex)

e.g. systemic lupus

94
Q

What is the type 4 hypersensitivity reaction?

A

Cell dependent (T cells & macrophage)

95
Q

What are 4 clinical indicators of an allergy?

A
  1. Skin - swelling, itching, redness
  2. Airways - excessive mucus production, bronchoconstriction
  3. GI - abdominal bloating, vomiting, diarrhoea
  4. Anaphylaxis - airway, breathing, circulation

SAGA

96
Q

Explain steps in an allergic response?

A
  1. Binding of IgE to its high affinity receptor
  2. Receptor cross linking
  3. Mast cells activated
  4. Granules released - histamine and cytokines
  5. Cytokines induce a Th2 response
97
Q

What chemicals do mast cells release immediately?

A
  1. Histamine - arteriolar dilation, capillary leakage
  2. Chemotactic factors - some cytokines
  3. Proteases - try-taste, chymase
  4. Proteoglycans
98
Q

What chemicals does mast cells release within a few minutes?

A
  1. Leukotrienes - capillary endothelial contraction with vascular leakage
  2. Prostaglandin D2 - potent inducer of smooth muscle contraction
  3. Platelet activating factor (PAF) - increases platelet aggregation
99
Q

What does mast cells release within a few hours?

A

Cytokines - IL-8, IL-5, IL-4, IL-13
(promote a Th2 response and lead to B cell class switching, IgE production)

100
Q

What the 3 activators of mast cells?

A
  1. Indirect activators (via IgE)
    a) allergens
    b) Bacterial/viral antigens
  2. Phagocytosis of enterobacteria
  3. Direct activators
    a) cold/ mechanical deformation
    b) aspirin, latex
101
Q

Define atopy in immunology.

A

A hereditary predisposition to the development of immediate hypersensitivity reactions against common environmental antigens

(tendency to develop allergies)

102
Q

What 5 things occur in the body in anaphylaxis?

A
  1. Mast cell or basophil activation
    • via IgE or direct activation
  2. CV
    • vasodilation, increased vascular permeability, lowered BP
  3. Respiratory
    • bronchial contraction, mucus
  4. Skin
    • Rash, swelling

Slow:
5. GI: pain, vomiting

103
Q

Explain what causes asthma?

A
  • complex inflammatory disease of the bronchi
  • triggered by allergens
  • can involve eosinophil influx into lungs
  • involved IgE
104
Q

How is chronic asthma different?

A
  • Non-Th2 T cell mechanisms in chronic asthma
  • CD8 (regulatory) T cells control eosinophil responses
  • similar to type 4 hypersensitivity
105
Q

What happens to IgE receptors when a ‘threat’ is identified?

A

the receptors cross link

106
Q

What is the main IgE receptor cell?

A

Mast cells

107
Q

What is the role of cytokine release in an allergic response?

A

Induce a Th2 response

108
Q

Give 5 treatments fo allergy and hypersensitivity.

A
  1. Avoid allergens.
  2. Desensitisation (immunotherapy, some risks).
  3. Prevent IgE production (interfere with TH2 pathway).
  4. Prevent mast cell activation.
  5. Inhibit mast cell products (e.g. histamine receptor antagonists).
109
Q

What is cancer immunoediting?

A

When the immune system kills tumour cells changes are induced in the tumour, the tumour cells are ‘edited’ by natural selection. The tumour cells are then disguised from the immune system, they escape destruction and recurrence is possible.

110
Q

What are the 3 E’s of cancer immunoediting?

A
  1. Elimination
  2. equilibrium
  3. escape
111
Q

Define allorecognition.

A

The ability of an organism to distinguish its own tissues from those of another. Recognition of non-self antigens.

112
Q

Describe the immune responses to detection of transplant graft antigens.

A
  1. Innate immune response is activated.
  2. T cell mediated cytotoxicity.
  3. Ab mediated cytotoxicity.
  4. Hypersensitivity.
  5. Tolerance.
113
Q

What activates the classical complement pathway?

A

Antibodies

114
Q

Briefly describe the classical complement pathway.

A
  1. Antibody binds to antigen on pathogen
  2. C1 is activated by binding to antibody antigen complex
  3. C1s cleaves C4 -> C4a and C4b AND C2 into C2a, C2b
  4. C4b binds C2b forming C4b2b. C4b2b is a C3 convertase and is responsible for C3 -> C3a and C3b.
  5. C4b2b binds C3b forming C4b2b3b.
  6. C3 convertase splits C5 into C5a & C5b
  7. C5,6,7,8 and 9 also bind and eventually you get MAC formation.
  8. MAC is a pore like channel in a membrane. Makes a hole in pathogen causing lysis, killing pathogen.
115
Q

What compound prevents excessive activation of the classical complement pathway?

A

C1 inhibitor.
- C1 inhibitor leads to a negative feedback loop.

116
Q

What activates the lectin pathway?

A

Mannose binding protein.

117
Q

What activates the alternative pathway?

A

Bacterial cell walls and endotoxin.

118
Q

What are the 3 different pathways that make up the complement system?

A
  1. Classical.
  2. Lectin.
  3. Alternative.
119
Q

Briefly describe the alternative pathway.

A
  1. C3 reacts slowly with H2O forming C3(H2O).
  2. C3(H2O) binds factor B. This becomes a substrate for cleavage by factor D.
  3. Factor B is split into Bb and Ba.
  4. Bb sticks to C3(H2O) forming C3(H2O)Bb.
  5. C3(H2O)Bb is a C3 convertase that cleaves C3 into C3b and C3a.
  6. C3b then binds to pathogens and causes opsonisation for improved phagocytosis. Also leads to MAC formation.

Non-specific as starts with C3 binding directly to pathogen instead of antibody binding to antigen.

120
Q

Which complement plasma proteins have opsonic properties when bound to a pathogen?

A

C3b and C4b

121
Q

What is the function of MAC in a pathogens’ membrane?

A

MAC is a leaky pore like channel. Ions and water pass through the channel and disrupt the intracellular microbe environment -> microbe lysis.

122
Q

Describe the lectin pathway.

A
  1. Mannose Binding lectin (MBL) binds to carbohydrate on certain microorganisms
  2. Activates MASP
  3. MASP binds to C1
  4. Continues the same way as the classical complement pathway
123
Q

Which complement plasma proteins are pro-inflammatory and cause chemotaxis and activation of neutrophils and monocytes etc?

A

C3a and C5a.

124
Q

Define anaphylaxis.

A

A severe and potentially life-threatening reaction to a trigger such as an allergy.
Sudden onset and rapid progression of symptoms. Life threatening airway and/or breathing and/or circulation problems.

125
Q

What are the signs and symptoms of anaphylaxis?

A
  • Occurs within minutes and lasts 1-2 hours
  • Vasodilation
  • Increased vascular permeability
  • Bronchoconstriction
  • Urticaria (hives)
  • Angio-oedema (rapid, oedema, or swelling, of the area beneath the skin or mucosa)
126
Q

What are common triggers of anaphylaxis?

A
  1. Food – peanuts, nuts, fish, shellfish, eggs, milk, sesame
  2. Venom – bee and wasp stings
  3. Drugs – antibiotics, opioids, NSAIDs, muscle relaxants
  4. Contrast agents – used in x-rays
  5. Latex – gloves
127
Q

Explain the pathophysiology of anaphylaxis?

A

Type 1 hypersensitivity reactions are IgE mediated.

  1. Must have had previous exposure, during which IgE antibodies where made.
  2. On re-exposure the IgE binds to high affinity IgE receptors on the surface of mast cells and basophils.
  3. Primed to react the next time the cells come into contact with the allergen
  4. Cross linking of IgE on the cell surfaces causes signalling cascade - rapid cellular degranulation and liberation of chemical mediators
  5. These chemical mediators are: histamine, protease enzymes, proteoglycans, prostaglandins, leukotrienes and chemotactic factors
  6. Reaction of antigen with IgE on mast cells also stimulates synthesis and release of platelet activating factor, leukotrienes and prostaglandins.
128
Q

What are the 2 types of anaphylaxis?

A

Immunological anaphylaxis
- prior exposure
- IgE antibodies formed

Non-immunological
- don’t involve IgE
- Don’t involve prior exposure
- common triggers: NSAIDs, anaesthetics

129
Q

Explain the effect of each of the symptoms of anaphylaxis.

A
  • Decreased oxygen saturation  increased mucous secretion, increased bronchial smooth muscle tone, airway oedema reduce ability to respire
  • Reduced lung expansion  Smooth muscle spasm in resp tract
  • Increased HR  vasodilation, increased vascular permeability
  • Increased temp 
  • Itchy  due to excitation of unmyelinated C-fibre
130
Q

How does adrenaline work in anaphylaxis?

A
  • Inject at anterolateral aspect of middle third of the thigh
  • Works on alpha 1, beta 1, beta 2 receptors.
  • Alpha 1  vasoconstriction, increase total peripheral resistance, increase blood pressure
  • Beta 1  positive ionotropic &isotopic effects stimulating heart rate
  • Beta 2  dilate bronchial tree, bronchodilation, reduces oedema
131
Q

What other treatments should you give for anaphylaxis?

A
  1. Establish airway  increase alveolar oxygen conc to overcome the hypoxia due to bronchospasm, reduced ventilatory effort, and interstitial oedema in the lungs
  2. Give High flow oxygen
  3. IV fluid challenge  help restore the circulating volume and therefore the stroke volume thus increasing the cardiac output
  4. Chlorphenamine  after initial resus. An antihistamine which blocks the histamine 1 receptor thus blocking the action of the histamine released during anaphylaxis.
  5. Hydrocortisone  after initial resus. Suppresses prostaglandins and leukotriene mediators, inflammatory cell recruitment and migration are inhibited. Vasoconstriction reduces leakage from the blood vessels.
  6. Apply monitoring  pulse oximetry, ECG, BP
132
Q

Explain why a second dose of adrenaline might be required.

A

Adrenaline has a short half life therefore a second dose may be required if the symptoms of not initially respond or get worse.

Biphasic anaphylaxis = recurrence of anaphylaxis after appropriate treatment with no additional exposure to allergen.
Can be 1 to 72 hrs after the initial attack and another dose of adrenaline is needed.

133
Q

What confirmatory blood test is required for anaphylaxis?

A

Serum mast-cell tryptase:
- can be measured in cases of anaphylaxis, particularly to clarify diagnosis where ambiguity exists.
- Tryptase is the preferred marker for demonstrating mast-cell degranulation (histamine elevation, for example, is very transient – lasts a short time).
- Levels of serum tryptase (mast cell specific protease) peak at one hour after an anaphylactic reaction and remain elevated for 6 hours

134
Q

What is the primary function of alpha 1?

A

Vasoconstriction

135
Q

What is the primary function of alpha 2?

A

Pre-synaptic inhibition
- inhibits release of NAD

136
Q

What are the primary functions of Beta 1?

A
  1. Increased cardiac effects e.g. force, rate and conduction
  2. Increased renin secretion
137
Q

What are the primary functions of beta 2?

A
  1. Bronchodilation
  2. vasodilation
138
Q

What are the primary functions of beta 3?

A
  1. Increase lipolysis
  2. bladder retention
139
Q

What the types of IgE receptors and where are they found?

A

Low affinity IgE receptors = expressed on B cells

High affinity IgE (FcεRII) = expressed on mast cells & basophils

140
Q

What is the function of GABA receptors?

A
  • used in anxiety
  • in CNS
  • many different drugs bind to different places on the receptor e.g. benzodiazepine, ethanol, barbiturates
141
Q

What are the functions and locations of the different types of histamine receptors?

A

H1 = line blood vessels in heart, smooth muscle cells (control smooth muscle contraction + vasodilation > allergies, IgE)
H2 = parietal cells, gastric acid secretion
H3 = In CNS - regulate neurotransmitters in brain
H4 = in T cells, mast cells and eosinophils

142
Q

What are the features of all the different TLR’s?

A

TLR 2 = detects gram + & TB
3 = intracellular
4 = detects LPS on gram -
5 = flagellin
6
7 = single strand RNA, intracellular
8 = intracellular
9 = non methylated DNA + intracellular

143
Q

Which TLR are intracellular?

A

3, 7, 8, 9

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