General Flashcards

1
Q

What is Apostasis?

A

Removing cells that have died of natural causes

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2
Q

When does Apostasis normally occur?

A

Embryonic development and ageing

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3
Q

What is the main overall purpose of Apostasis?

A

Maintain cell populations within tissues.

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4
Q

What is adaptive immunity and what allows it to be adaptive?

A

It is specific due to the presence of T&B lymphocytes

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5
Q

What is innate immunity?

A

Non-specific - natural immune system

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6
Q

What type of immunity does the skin cause and how does it do this?

A

Innate immunity. Protects underlying tissues from microbes.

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7
Q

What is the technical name for sweat glands and what are their purpose?

A

Sudoriferous (sweat) hands produce lysosomes that degrade peptidoglycands.

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8
Q

What are peptidoglycands composed of and what are their purpose?

A

Essential component of a bacterial cell wall - prevents the bacterial cell from bursting due to turgor pressure.
Mesh-like macromolecule composed of glycan chains and short peptides.

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9
Q

What is the Stratum Corneum and what is its purpose?

A

Outer layer or flat, dead cells on the skin which are filled with keratin and provide a physics barrier to invasion, abrasion and dehydration.

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10
Q

Name a type of non-pathogenic bacteria that surpasses virulent bacteria.

A

Commensal bacteria. Non-pathogenic bacteria.

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11
Q

Where is commensal bacteria found - examples.

A

Skin, mouth, reproductive regions, gastrointestinal tracts.

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12
Q

How do commensal bacteria act as a form of innate immunity?

A

They attach to the skin therefore blocking areas where pathogenic bacteria can attach. They also compete with pathogenic for nutrients so less nutrients are available on the skin for pathogenic bacteria. They also release antibacterial substances such as colicins.

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13
Q

What antibacterial substances do commensal bacteria release?

A

Colicins-proteins, short fatty acids.

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14
Q

How do mucus membranes act as a form of innate immunity?

How is mucus able to be a form of immunity.

A

Tracts lines with mucus membranes trap and protect us against microbes. Mucus is a long branched carbohydrate and is therefore viscous and able to trap foreign bodies for phagocytosis.

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15
Q

How do hairs in the nose act as a type of innate immunity?

A

Increase surface area and therefore increase trapping potential.

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16
Q

Name types of innate immunity (general).

A

Mucous membranes, hairs, acid, flushing, commensal bacteria, skin, eyes, ears, mouth.

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17
Q

What is secreted from the ears as part of innate immunity?

A

Cerumen waxy secretion from the sebaceous glands.

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18
Q

What is produced by a humoural immune response?

A

Antibodies

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19
Q

What is produced by a cell-mediated immune response?

A

Cytotoxic T lymphocytes.

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20
Q

Where does Hematopoiesis occur?

A

The hematopoietic system (bone marrow, liver, spleen etc.)

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21
Q

When does Hematopoiesis begin?

A

Embryonic development.

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22
Q

What (in general) is hematopoiesis?

A

Replacing old red blood cells with new red blood cells.

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23
Q

Name the 2 main categories of phagocytic cells

A

Granulocytes and Macrophages

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24
Q

Name 2 types of granulocytes and any further details.

A

Neutrophils- Highly active, short life span. Monocytes- Travel round the body, develop into macrophages.

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25
Q

Name two types of macrophages and any further details.

A

Wandering macrophages- travel as monocytes around the body, do chemotaxis during inflammation.
Fixed Macrophages- Present in most organs.

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26
Q

What are the 2 ways that a phagocyte attaches to a bacterium?

A

Antibody is made that attaches to the bacterium. A receptor present on the phagocyte then attaches to the antibody and they bind.
OR
A complement molecule attaches to the bacterium and then to a complement receptor on the phagosome.

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27
Q

What is a Phagolysosome?

A

A digestive vesicle formed within a cell by the fusion of a phagaosome containing ingested material and a lysosome containing hydrolytic enzymes.

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28
Q

What are the 2 killing mechanisms of Phagoytosis?

A

Oxygen-dependent and Oxygen-independent

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29
Q

What happens during oxygen-dependent killing mechanisms of phagocytosis?

A

Lysosomes degrade bacterial cell walls, cationic proteins cause pH to fall, defensives bind to bacterial membranes and form pores, acid hydrolase enzymes degrade carbohydrates.

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30
Q

What are the 3 ways that Apoptosis can occur?

A

Intrinsic pathway
Extrinsic pathway
Apoptosis Inducing Factor

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31
Q

Describe the intrinsic apoptosis pathway.

A

Cell damaged- BAX released- Inhibits release of BCL2 from mitochondria membrane. BAX punctures holes in outer mitochondrial membrane. Cytohrome C released into cytoplasm and causes apoptosome to form. Activates Caspase 9. Kills organelles.

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32
Q

Describe the extrinsic apoptosis pathway.

A

Death receptors (integral membrane proteins) bind to death activating molecules outside the cell. Caspase 8 activated inside cell. Destroys organelles.

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33
Q

How does the Apoptosis inducing factor theory work?

A

AIF is transferred into the cytoplasm of the cell and then into the nucleus, binding to the genetic material if a cell is damages.
Destroys DNA

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34
Q

Where is apoptosis inducing factor found ?

A

Intermembrane space between the inner and outer mitochondrial membranes.

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35
Q

How do macrophages generally work in terms of B cells?

A

Macrophages engulf and break down different types of pathogens. They then present the antigens from the pathogen on their own membrane. Complimentary B lymphocytes bind to the antigen receptor sites and cell mediated immunity will occur. This cell mediated immunity activates helper T cells to differentiate into plasma and memory B cells. Allows many antibodies to be formed that are complimentary to the initial antigen on the pathogen.

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36
Q

Where are B lymphocytes produced?

A

Bone marrow

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37
Q

Where can an example of humoural immunity be found?

A

In Macrophages.

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38
Q

Where are T lymphocytes produced and matured?

A

Produced- Bone marrow

Matured- Thymus

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39
Q

What happens to T-lymphocytes when the body is infected and how does cell mediated immunity then occur?

A

T-lymphocutes differentiate into helper T cells and cytotoxic T cells. The cytotoxic T cells travel to the site of infection and use antibodies on their surface to bind to antigens on the pathogens surface. Then then release perforin proteins which kill the pathogen cells. T memory cells are also formed as well as suppressor cells that can regulate the immune response.

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40
Q

Where does Hematopoeisis occur?

A

Bone marrow

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41
Q

What type of cells to Haematopoeitic stem cells differentiate into?

A

Myeloid cell types or Lymphoid cell types.

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42
Q

What types of Lymphoid cells are present in Haematopoeisis?

A

T lymphocytes and B lymphocytes

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43
Q

Name a type of Myeloid cell

A

Erythrocyte, Megakaryocyte, Monocyte, Neutrophil, Basophil, Eosinophil.

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44
Q

What type of cell is a Megakaryocyte and what is its function?

A

Myeloid cell - gives off cytoplasm to form platelets.

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45
Q

Describe the naming difference in T and B cells before and after they have matured.

A

Immature- B Lymphoblasts and T Lymphoblasts.

Mature - B Lymphocytes and T Lymphocytes.

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46
Q

What are dendritic cells and where are they found?

A

A type of immune cell found in the sin, gut, lungs, digestive tract etc.

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47
Q

Explain in general how an enzyme- cascade system works and what it is.

A

An in-active enzyme is activated. This newly activated enzyme then activates another enzyme and the cycle continues.
The initial effect is amplified.

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48
Q

What are 4 major cascade systems in the blood?

A

Blood clotting
Kinin
Firbrinolytic
Complement

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49
Q

Draw a flow diagram showing how the alternative complement system causes immunity based on C3.

A

IN NOTES !!!

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50
Q

What are the 3 general outcomes of the alternative complement pathway.

A

Cytolysis, phagocytosis, inflammation.

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51
Q

Give an example Opsonisation and its benefits.

A

C3b receptors on the macrophages and C3b proteins on the phagocyte are complimentary and therefore bind. This aids the phagocytosis process.
Benefits = drastically reduces the % of the phagocyte present in the organism as compared with normal phagocytosis.

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52
Q

Where are most complement enzymes before activation?

A

In the blood as pre-enzymes.

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53
Q

What is the general onset time and duration of chronic inflammation?

A

Slow onset, long duration

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54
Q

What is the general onset time and duration of acute inflammation?

A

Rapid onset, short duration

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55
Q

What are the 3 pathways of the complement system?

A

Alternative, Classical, Lectin

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56
Q

What usually causes acute inflammation ?

A

Microbes, chemical irritants, physical trauma, exposure to extreme temperature.

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57
Q

What cell type is used to combat acute inflammation ?

A

Neutrophils

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58
Q

Where are neutrophils activated during the acute inflammation process?

A

In the endothelium cells lining blood vessels.

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59
Q

What are the features of activated neutrophils in the acute inflammation system?

A

Increased receptors for chemoattractants, prostaglandins , leukotrienes and FCs. As well as more complement proteins.

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60
Q

How does activation of neutrophils affect metabolic activity and hows this helpful for immunity.

A

Neutrophils stimulate metabolic activity which produces oxygen and nitrogen containing intermediates such as hydrogen peroxide which are harmful chemical mediators used to kill the pathogens.

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61
Q

Outline to sequence of events in acute inflammation.

A

Pathogen enter tissue and cause damage.
Mast cells come into. contact with the pathogen and release histamine, prostaglandins and leukotrienes.
Histamine causes violation of arterioles, increasing blood flow.
Capillar permeability increases, causing oedema.
Complement proteins leave the capillary and are activated by the phagocyte.
Chemotaxis of neutrophils to the affected area.
Killing of pathogen by neutrophils - phagocyte.
Tissue repair

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62
Q

How are prostaglandins and Leukotrienes stored ?

A

They cannot be stored so must be made from scratch during the acute inflammation process.

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63
Q

What is oedema?

A

The osmotic balance between the blood and tissue in question is damaged. Molecules such as plasma proteins are able to move through membranes and causes swelling of the tissue.

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64
Q

What tissue damage can occur due to acute inflammation?

A

Tissue damage can occur but is usually very minor and impermanent.

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65
Q

What systems are in place to limit the tissue damage during acute inflammation?

A

Chemicals such as TGF beta stop and slow the inflammatory response.

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66
Q

What repairs are made after acute inflammation damage?

A

Fibroblasts are stimulated to repair the extra-cellular matrix for cells and produce collagen to repair tissue.

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67
Q

What are the symptoms of the inflammation (Latin name and explanation ).

A
Calor - heat
Dolor - Pain
Rubor - Redness
Tumour - Swelling
Functio Laesa - loss of function
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68
Q

What is extravasation in general terms?

A

How neutrophils move from the blood vessels to the site of damage.

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69
Q

What is the purpose of the vascular endothelium in cells?

A

Acts as a gateway regulating movement of molecules between cells and the blood.

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70
Q

What type of molecules are vital for Extravasation?

A

Cell adhesion molecules (CAMs).

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71
Q

Explain the process of Extravasation and how it allows neutrophils to reach the invaded site.

A

The mucin molecules on neutrophils and the E-selectin molecules on the endothelial cell bind - low affinity binding. This causes the endothelial cell to release Chemokine. Chemokine activates integrin and therefore allows a firm bonding between the neutrophil and endothelial cell using CAMS. The neutrophils can then migrate to the affected area as hey are attracted by chemoattractants.

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72
Q

What are interferons (general)?

A

Proteins produced by certain types of cells infected with viruses.

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73
Q

What is the main function of interferons and are they specific?

A

Non-specific

Interferons inhibit viral replication.

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74
Q

What are the functions of type 1 interferons and what are the type 1 interferons?

A

Alpha and beta interferons. Suppress tumours and metastasis.

Used to trat Kaposi’s sarcoma, genital warts and hepatitis C.

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75
Q

What is metastasis?

A

Abit of tumour splits off and goes to another part of the body to use a secondary tumour.

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76
Q

What are the type 2 interferons and what are their functions?

A

Gamma interferons.

Activates neutrophil and macrophages to enhance phagocytosis and the inflammatory process.

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77
Q

What cell types are the 2 interferons secreted from?

A

Natural killer cells and cytotoxic T cells.

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78
Q

How do interferons work to inhibit viral replication?

A

Interferons diffuse into neighbouring cells and bind to surface receptors. Interferons stimulate tissue cells to synthesise anti-viral proteins that inhibit viral replication.

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79
Q

By what method do natural killer cells kill cells?

A

Cytolysis and they also induce apoptosis.

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80
Q

What cells differentiate into natural killer cells?

A

Common lymphoid progenitor cells - innate lymphoid cells - natural killer cells.

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81
Q

Where are natural killer cells found?

A

Lymph nodes, spleen, bone marrow, blood.

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82
Q

Why are natural killer cells so fast acting and powerful?

A

They produce and respond to the stimulus to create a magnifying effect.

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83
Q

How do natural killer cells cause cytolysis?

A

They secrete perforin. Perforin forms holes in the plasma membranes of cells. Plasma proteins can therefore move into and out of the cell and change the osmotic gradient. A Lot of water moves into the cell by osmosis and causes osmotic lysis.

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84
Q

What types of cell are defensives active against?

A

Bacteria, fungi and some viruses.

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85
Q

How do defensives kill off pathogens?

A

They form pores in target cells and therefore affect osmotic potential - leading to osmotic lysis.

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86
Q

What are cells are pattern recognition receptors on and what pattern types do they recognise?

A

Proteins on innate immune cells and epithelial cells.

They recognise pathogen-associated molecular patterns and damage-associated molecular patterns.

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87
Q

What is the purpose of patter recognition receptors in the inflammatory process?

A

These proteins bind to pathogens and release inflammatory cytokines.

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88
Q

What response accompanies the acute phase response?

A

The local inflammatory response.

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89
Q

What happens during the acute phase response?

A

Rapid rise in the levels of acute phase serum proteins. These proteins limit the release of and toxidity of bacteria They bind to bacterial phospholipids, activate complement proteins and therefore enhance phagocytosis.

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90
Q

What stimulates the release the release of acute phase serum proteins?

A

Cytokines and macrophages.

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91
Q

Where are acute phase serum proteins made?

A

The liver

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92
Q

What is the purpose/ function of acute phase serum proteins?

A

They limit the release and toxicity of bacteria by binding to bacterial phospholipids, activating complementing bacteria and therefore enhancing phagocytosis.

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93
Q

What are the effects of the acute phase response ?

A

Increased body temperature (not ideal for pathogens), ACTH (hormone released which causes cytosol to be made and activate the white blood cells).

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94
Q

Where is ACTH hormone made and released?

A
Made = pituitary gland
Released = adrenal glands
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95
Q

What is the effects of ACTH being released into the adrenal glands?

A

Activates which blood cells.

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96
Q

What are the 2 mechanisms for specific immunity?

A

Humoral immunity

Cell mediated immunity

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97
Q

What does the specificity of humoral immunity rely on?

A

Antibodies

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98
Q

What does the specificity of cell mediated immunity rely on?

A

T cells

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99
Q

Define antigen .

A

Any substance that when introduced to the body, is recognised as foreign and is capable of inducing a specific immune response .

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100
Q

Define immunogenicity .

A

The ability to induce an immune response .

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101
Q

What is produced when a B cell comes into contact with an immunogen?

A

Effector B lymphocytes and Memory B cells .

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102
Q

What is produced when T cells come into contact with an immunogen?

A

Effector T lymphocytes and T memory cells are produced .

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103
Q

Is an immunogen always an antigen?

A

Yes

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104
Q

Is an antigen always an immunogen?

A

No

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105
Q

What factors is immuogenicity determined by?

A

Degree of foreigness, molecular size, chemical composition and heterogeneity, susceptibility to antigen processing and presentation .

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106
Q

How does degree of foreigness affect immunogenicity?

A

The more foreign the microbe is and the less similar it is to body cells, the more likely to trigger an immune response .

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107
Q

How does phylogenetic evolution affect immunogenicity of a microbe?

A

As phylogenetic distance increases, the more likely the foreign body is to cause an immune response as it appears less like a self component .

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108
Q

Why do some self-components trigger an auto immune response?

A

Some self-components are sequestered (hidden) so may be recognised as foreign if they enter other regions of the body .

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109
Q

How does molecular size affect immunogenicity?

A

The larger the immunogen, the larger the immune response .

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110
Q

How do aromatic amino acids affect immunogenicity?

A

Increase immunogenicity .

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111
Q

What type of stereo-isomers are non-immunogenic?

A

D isomers because they cannot be degraded .

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112
Q

How does solubility increase immunogenicity?

A

The more insoluble a microbe, the more it aids phagocytosis and therefore the more it aids immunogenicity .

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113
Q

What varies the effects of the immunogen on an individual

A

The genotype of the recipient, immunogen dosage, imunogen route, adjuvants .

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114
Q

What are adjuvants in terms of immunogens ?

A

They work with the immunogen to enhance receptors .

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115
Q

Define Atnigenicity .

A

The ability to combine with products of the immune response .

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116
Q

What are endogenous antigens and what cells are they recognised by?

A

Recognised by Cytotoxic T cells .

Originate inside the body and presents antigens on its surface .

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117
Q

What are exogenous antigens?

A

Originate outside the body and are recognised by T helper cells .

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118
Q

Give an example of an exogenous microbe .

A

Bacterial infections .

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119
Q

What receptors do B lymphocytes have to recognise antigens?

A

Have B cell antibodies on their surface which act as antigen receptors .

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120
Q

What receptors do T lymphocytes have on their surface to recognise antigens?

A

T cell antigen receptors .

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121
Q

What is the advantage of having large antigens?

A

The larger the antigen the larger the binding site for T/B lymphocytes .

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122
Q

Which polysaccharides do/ don’t trigger an immune response?

A

Small dont

Large do

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123
Q

What are epitopes?

A

The site on an antigen molecule where the antibody binds .

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124
Q

How many epitopes sites can an antibody bind to?

A

1 - they are highly specific .

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125
Q

How many epitopes do antigens have on their surface and why?

A

Many because this allows the effective production of many different antibody types to allow an effective immune response .

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126
Q

What are haptens?

A

Molcules which are too small to initiate an immune response .

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127
Q

How can haptens be made to cause an immune response?

A

Haptens can be linked to carrier molecules to trigger an immune response and react with an antibody .

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128
Q

Are haptens antigenic and immunogenic when linked with a carrier molecule?

A

They are antigenic but not immunogenic .

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129
Q

Define antibodies .

A

A group of protein globuin glycoproteins and immunoglobulins present in the blood plasma that combine with the antigenic determinant that triggered its prodicton .

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130
Q

When is the constant region for the antibodies structure the same?

A

The same for antibodies of the same class .

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131
Q

How many and what type of chains is the antibody structure composed of ?

A

2 identical inside heavy chains and 2 identical outside light chains .

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132
Q

How are the chains of the antibody structure held together?

A

The 2 heavy chains and held by 2 disulphide bridges . The heavy chains are attached to the light chains by 1 disulphide bridge .

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133
Q

What causes the Y shape of he antibodies .

A

Hinge regions on the heavy chains which enable flexibility .

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134
Q

What are variable regions of the antibody structure?

A

Tips of the heavy and light chains which act as antigen binding sites .

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135
Q

What are hypervariable regions of the antibody structure?

A

Very tip of the light and heavy chains .

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136
Q

How many hypervariable regions do most antibodies have?

A

2

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137
Q

What is a unique feature of the IgG antibody?

A

The only antibody that can cross the placenta .

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138
Q

What is the purpose and main function of IgG antibodies?

A

Protect us against bacteria and viruses - high affinity to microbes at epitope sites and trigger complement system, enhance phagocytosis and neutralise toxins .

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139
Q

Wha is the general function of IgA antibodies?

A

Provides localised protection mucus membranes .

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140
Q

What is the general function of IgM anitbodies?

A

Causes lysis of microbes and helps agglutinated of red blood cells .

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141
Q

In what ways do antigen-antibody complexes neutralise or eliminate antigens?

A

Activation of complement systems by the classical pathway, phagocytosis through oposonisation, neutralisation by cross-linking molecules of toxins or viruses .

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142
Q

How are monoclonal antibodies made?

A

Antibody-producing B cells fuse with myeloma cells . This creates a hybridoma which is immortalised and antibody producing .

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143
Q

How are monoclonal antibodies used to find cancers?

A

Toxins are often placed on the tail of monoclonal antibodies and the toxins are then delivered directly to the cancer .

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144
Q

What causes the precipitation to occur in the precipitation ring practical?

A

The antigens (with 2 or more epitopes) become cross linked by the use of complimentary antigens to form a lattice. The antigens and antibodies must be in equal ratios.

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145
Q

What must be a feature for the precipitate to form in the precipitation ring practical?

A

The antigens and antibodies must be present in the same concentration.

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146
Q

Why is it necessary to use a series of antigen dilutions in the precipitation ring practical?

A

To ensure a tube contains a zone of equivalence (precipitate) for optimum complex formation. Enables semi-quantitate results to be recorded. Required due to the polyclonal nature of the antibodies.

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147
Q

What factors does the forming of a precipitate depend on in the precipitate ring practical?

A

The affinity of the antigen to the antibody - higher affinity = greater precipitate.
Ratio of antibody to antigen - must be in equal concentrations.

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148
Q

Why may no precipitate be present in the precipitate ring reaction?

A

If the optimum ratio of antibodies to antigens is not present no lattice and therefore no precipitate will form. The antigen must be in equal concentration to the antibody.

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149
Q

Define precipitin.

A

Soluble antibodies which react with soluble antigens to form a precipitate.

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150
Q

Define Precipitinogen.

A

Soluble antigens which induce the formation of precipitin.

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151
Q

Define lattice in terms of the precipitin ring practical.

A

The cross linking of antigens and antibodies to form and immunocomplex.

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152
Q

What is the equivalence zone in the precipitate ring reaction?

A

The zone where the concentration of antibodies and antigens is equal. A immunocomplex lattice can form. Precipitate is present.

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153
Q

What is the basic difference between Geel diffusion occurring in Oudin tubes and Ouchterlony plates?

A

Oudin tubes used single, one directional diffusion.

Ouchterlony plates use 2D diffusion.

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154
Q

What is the clinical significance of febrile antibodies?

A

Used to diagnose infections and diseases such as haemolytic anaemia.

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155
Q

Why does Agar jelly resist contamination with bacteria?

A

Agar is a polymer made up of subunits of galactose and red algae so cannot be easily degraded by micro-organisms.

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156
Q

What are semi-quantitative results?

A

E.g “Less than 5” “Between 5 and 20” “Greater than 20”.

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157
Q

Which method (Ouchterlony or Precipitation ring reaction) produces a more stable precipitate?

A

Ouchterlony

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158
Q

Are Ouchterlony or precipitation ring reactions quicker?

A

Precipitation

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159
Q

How does agglutination differ from precipitation reactions?

A

An insoluble antigen is used in agglutination whereas precipitation methods use soluble antigens.

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160
Q

Do precipitation methods use soluble or insoluble antigens and antibodies?

A

Both are soluble but form an insoluble complex.

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161
Q

Define inflammation (acute).

A

The local response of living tissue to any infectious agent.

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162
Q

Compare the onset times of acute and chronic inflammation.

A

Acute - rapid

Chronic - slow

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163
Q

Compare the cells used for acute and chronic inflammation.

A
Acute = Neutrophils
Chronic = Lymphocytes, Monocytes and macrophages.
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164
Q

Compare the type of tissue injury which induces acute and chronic inflammation.

A
Acute = Mild
Chronic = Severe and processingly worsening
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165
Q

What are the 5R’s / 5 steps to an inflammatory response?

A

Recognition (of the injurious agent)
Recruitment ( of inflammatory cells - leukocytes)
Removal (of the injurious agent)
Regulation (of the inflammatory response)
Resolution / repair

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166
Q

What are the two main overall processes that occur as part of acute inflammation?

A

Vascular changes

Cellular events

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167
Q

What are the vascular changes that occur during acute inflammation?

A

Vasodilation and increased vascular permeability.

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168
Q

How is vasodilation caused during acute inflammation?

A

Histamine hormone is used to expand the arterioles and increase the blood flow. This causes the tissue to become red and warm.

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169
Q

What process in acute inflammation causes the red and hot symptoms?

A

Vasodilation

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170
Q

What are the overall purposes of vasodilation and increased vascular permeability in acute inflammation?

A

The blood becomes more viscous so blood flow is slowed. This leaves time for the engorgement of small vessels.

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171
Q

What are the 4 ways that vascular permeability increases during acute inflammation?
Explain each one.

A

Contraction of the endothelial cells - causes gaps between endothelial cells to become larger and allows leakage of fluid, blood and proteins to move into the extravascular space.
Direct endothelial damage such - toxins and burns cause endothelial damage allow leakage.
Injury of endothelial cells due to leukocytes - neurophils adhere to the endothelial cells and damage them. Leads to leakage.
Transcytosis- increased transport of fluids and proteins in the intracellular channels. The channels are stimulated by vascular endothelial growth factors which promote leakage.

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172
Q

Explain how transcytosis can cause vascular permeability to increase.

A

There is increased transport of fluids and proteins into the intracellular channels. The channels are stimulated by vascular endothelial growth factors which promote leakage.

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173
Q

What are leukocytes?

A

A type of white blood cell. Often used in the inflammatory response.

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174
Q

What cellular events occur to cause acute inflammation?

A

Recruitment of Leukocytes.

Activation of Leukocytes leading to the process of destruction of invading cells and production of mediators.

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175
Q

What are the stimuli for acute inflammation.

A

Tissue necrosis - cells released from the dying cell site act as stimuli.
Infection
Trauma ( due to physical or chemical agents)
Foreign bodies (splinters etc)
Immune reactions

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176
Q

What is tissue necrosis?

A

The passive breakdown of order structure and functions of a tissue resulting in irreversible damage.

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177
Q

How are acute inflammation stimuli recognised by the host in general terms ?

A

They are recognised by receptor on antigen presenting cells and epithelial cells.

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178
Q

What 2 types of receptors recognise acute inflammation stimuli?

A

Toll like receptors

Inflammasomes

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179
Q

What do toll like receptors detect as part of the acute inflammatory response?

A

They detect microbial stimuli and pathogen products.

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180
Q

Where are toll like receptors present?

A

Plasma membrane and endosomes

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181
Q

What are endosomes?

A

Membrane bound vesicles.

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182
Q

What is the outcome of the use of toll like receptors in acute inflammation?

A

Results in the production of inflammatory mediators.

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183
Q

What do inflammasome receptors detect as part of the acute inflammatory response?

A

They recognise multi protein cytoplasmic complexes and products of dead cells.

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184
Q

What is the outcome of using inflammasome receptors in the acute inflammatory response?

A

They activate caspace-1 which activates mediators of leukocyte recruitment. The recruited leukocytes then phagocytose and destroy the injurious agent or dead cells.

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185
Q

Outline the life cycle of a B lymphocyte duding interphase.

A
G0- B lymphoid is small and nieve. 
Antigens activate B lymphocyte. 
G1- Genes within B lymphocyte are activated and DNA is synthesised. 
Lymphoblast S produced. 
G2 - Cell division.
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186
Q

What do B lymphocytes derive from and where are they produced?

A

Stem cells

Bone marrow

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187
Q

How do B lymphocytes move around the body?

A

Via the blood

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188
Q

Where are B cells stored ?

A

The lymphatic system

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189
Q

What part of the B cells allows activation by antigens?

A

B cells immunoglobulin on their membrane. This can be activated to induce differentiation.

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190
Q

How long do plasma cells generally survive for?

A

1-2 weeks

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191
Q

How long do memory cells generally survive for?

A

Decades

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192
Q

What do B lymphocytes divine into?

A

Plasma cells and memory cells

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193
Q

What are the 3 different types of lymphocytes ?

A

B cells, T cells, Natural Killer cells (NK cells).

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194
Q

Are B and T lymphocytes part of the specific or non-specific immunity?

A

Specific

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195
Q

Where do T and B cells migrate to from the bone marrow?

A

Lymphatic system

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196
Q

What are T and B cells activated by ?

A

Antigens

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197
Q

Are Natural killer cells part of specific or non-specific immunity?

A

Non-specific

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198
Q

Where are clusters of differentiation found?

A

Antigens on the surface of lymphocytes

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199
Q

How are CD antigens used to identify cell types which are present in a sample - outline the process.

A

Monoclonal antibodies are marked with fluorescent markers on their tail end. These monoclonal antibodies bind to the specific CD (cluster of differentiation) antigens on the lymphocyte surfaces.
The fluorescent colouring present will identify what cell types are present in the lymphocyte mixture because a colour complex is formed when the marked monoclonal antibody binds to a complimentary CD antigen.

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200
Q

What cell type are CD4 antigens used to identify?

A

Helper T cells

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201
Q

What cell type are CD8 antigens used to identify?

A

Cytotoxic T cells

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202
Q

What cell types are CD21 antigens used to identify?

A

B cells

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203
Q

Outline the life cycle of a T lymphocyte.

A

Stem cells differentiate into immature T cells in the bond marrow. These then migrate to the thymus gland via the blood.
In the thymus, the immature T cells differentiate in to cytotoxic, helper and regulatory T cells via a highly selective process.
They then travel via the blood to the thymus-dependent areas of the lymph nodes and spleen.
They remain here until being activated.

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204
Q

Which specific antigens can T lymphocytes recognise?

A

Antigens displayed alongside MHC molecules.

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205
Q

Which specific antigens can B lymphocytes recognise ?

A

All free antigens

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206
Q

What type of CD antigen markers do helper T cells have and what type of MHC antigens do they recognise?

A

CD4

MHC classII

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207
Q

What type of CD antigen markers do cytotoxic T cells have and what type of MHC antigens do they recognise?

A
CD8
MHC class I
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208
Q

What type of CD antigen markers do regulatory T cells have ?

A

Some have CD4 and are therefore MHC class II restricted. Others have CD8 and are therefore class I restricted.

209
Q

What are major histone complexes?

A

Tightly linked clusters of genes present in every mammalian species.

210
Q

Which chromosome are major histone complexes present on in humans?

A

6

211
Q

What are polymorphic genes?

A

There are multiple alleles for each genes

212
Q

What are halotype inherited genes?

A

A group of genes within an organism that have been inherited from only one parent.

213
Q

Where are polymorphic genes often present?

A

Oh major histone complexes.

214
Q

What does MHC stand for?

A

Major histone complexes.

215
Q

What type of antigens are presented to helper T cells?

A

Exogenous

216
Q

How do antigen presenting cells work?

A

They present a fragment of the antigen associated with an MHC molecule on their plasma membrane surface.

217
Q

What are endogenous antigens?

A

They original inside the body and create complexed with MHC class I proteins.

218
Q

What cell type are endogenous antigens recognised by ?

A

Cytotoxic T cells

219
Q

What are exogenous antigens?

A

They originate outside the body and create complexes with MHC class II proteins.

220
Q

What cell type are exogenous antigens recognised by?

A

Helper T cells

221
Q

Which MHC class do exogenous antigens create complexes with?

A

MHC class II

222
Q

Which MHC class do endogenous antigens create complexes with?

A

MHC class I

223
Q

What are the 3 types of antigen presenting cells.

A

Macrophages
Dendritic cells
B cells

224
Q

How do macrophages present antigens ?

A

Macrophages phagocytose and partially digest antigens which then combine with MHC class II proteins. The complex is then inserted into the macrophage plasma membrane where it is recognised by T helper cells. They can also present antigens which are un-associated with MHC molecules to B cells.

225
Q

How do dendritic cells present antigens?

A
They trap antigens on their surface and present them to T and B lymphocytes depending on their location. They are endocytic.  
Often create a complex with MHC class II proteins and therefore can be recognised by helper T cells.
226
Q

How do B cells present antigens?

A

In certain situations, B cells can perform macrophage functions of processing and presenting antigens to helper T cells after forming a complex with MHC class II. They also secrete Interleukin-I to help activate T cells.

227
Q

What type of MHC molecules are always carried on antigen presenting cells ?

A

Class II

228
Q

What is the overall, general purpose of cell-mediated immunity?

A

To kill foreign or abnormal cells.

229
Q

What are the 3 ways that cytotoxic T cells kill ?

Give a brief outline of each.

A

Cytolysis - release perforin
DNA fragmentation - Release lymphotoxin which fragments nuclear DNA.
Phagocytosis - Release gamma interferon which enhances phagocytic activity of macrophages.

230
Q

When do T cells move from their immature to mature form?

A

When they are activated by antigens.

231
Q

Outline the process of T cell activation for CD4 T cells.

A

TCR recognises molecules on the T cells and binds to the CD4 and MHCII molecules on the surface of the antigen presenting cell. This creates the first signal.
When the T cells are activated, interleukin-2 is released by the T cell and binds to specific receptors on the same T cell (autocrine).
T cells then undergo proliferation and differentiation to produce effector T cells and memory T cells.
Effector CD4+ T cells eventually become helper T cells.

232
Q

What are the differences between CD4 and CD8 T cell activation ?

A

CD4 - MHC II molecules and T effector cells become helper T cells.

CD8 - MHC I molecules and T effector cells become cytotoxic T cells.

233
Q

What is proliferation?

A

To multiply rapidly

234
Q

What would occur if costimulation of T cells didn’t occur?

A

T cells would remain in a prolonged state of inactivity known as anergy.

235
Q

What is anergy?

A

Absence of the normal immune response to a particular antigen - T cells are never activated.

236
Q

What is the purpose of costimulator molecules?

A

They allow T cells to adhere to the antigen presenting cell for a longer amount of time.

237
Q

What type of molecules are costimulator molecules?

A

Cytokines or a pair of plasma membrane molecules.

238
Q

What is the recruitment of leukocytes during acute inflammation controlled by?

A

Adhesion molecules and Chemokines

239
Q

What is the general purpose of Chemokines duding acute inflammation?

A

They arrant cytokines which aids migration of leukocytes to the site if inflammation.

240
Q

Name the steps of migration of leukocytes during acute inflammation.

A
Margination
Rolling
Adhesion
Diapedesis
Chemotaxis
241
Q

Outline the process of margination of Leukocytes during acute inflammation.

A

The blood has been slowed by vascular processes therefore leukocytes are able to move towards the periphery of the blood vessels and gather along the epithelial cells.

242
Q

Outline the process of rolling in migration of Leukocytes during acute inflammation.

A

Leukocytes bind to an epithelial cell. They then detached and bind to an epithelial cell further down the blood vessel.

243
Q

What is the rolling of Leukocytes in acute inflammation controlled by ?

A

P, E and L selectin molecules.

244
Q

Describe the binding of selectin molecules to Leukocytes.

A

Low affinity

245
Q

Outline the adhesion process of Leukocyte migration during acute inflammation.

A

Leukocytes express integrin proteins on their surface and endothelial cells present inter grin ligands. Intergrin molecules on the Leukocyte then bind to integrin receptors on the endothelial cells. This allows high affinity binding between the Leukocytes and the Endothelial cells.

246
Q

What are the 2 types of intern ligand?

A

Vascular cell adhesion molecules (VCAM-1)

Intracellular adhesion molecules (ICAM-1)

247
Q

Outline the Diapedesis process of migration of Leukocytes during acute inflammation.

A

Leukocytes squeeze between gaps in the endothelial cells by transmigration. The Leukocytes then secrete chemicals which break their basement membrane and allow them to move into the extra-vascular tissue.

248
Q

What is the Diapedesis process during migration of Leukocytes controlled by?

A

PECAM molecules - Plateles cell adhesion molecules

249
Q

Outline the mechanism for chemotaxis of leukocytes during acute inflammation.

A

Chemoattractants bind to specific receptors on the Leukocytes and cause polymerisation of actin and localisation of myosin. The Leukocytes then extend filopodia and are pulled towards the chemoattractant.

250
Q

What is meant by the term localisation?

A

The movement of a specific substance to a specific region.

251
Q

What is extending filopodia?

A

Migrating cells use cytoplasmic projections called micro spikes to form adhesions with the cell surface membrane and therefore move.

252
Q

What type of receptors are used to detect foreign bodies during acute inflammation?

A

Phagocytic receptors (Mannose receptors, Scavenger receptors, Opsonin receptors).

253
Q

What are the 3 types of phagocytic receptors used to detect foreign bodies in acute inflammation?

A

Mannose receptors, Scavenger receptors and Opsonin receptors.

254
Q

What are the purpose of mannose receptors during acute inflammation?

A

They bind to terminal mannose and residues of glycoproteins and glycoplipids which are found in microbial walls.

255
Q

What is the purpose of scavenger receptors in acute inflammation

A

They bind to modified low density lipid molcules found within lipids.

256
Q

What is the purpose of opsonin receptors in acute inflammation?

A

They recognise opsonins which are antibodies which bind to forming microorganisms and make them more susceptible to phagocytosis.

257
Q

What are opsonins?

A

Antibodies which bind to microorganisms and make them more susceptible to phagocytosis.

258
Q

What 3 main things can happen when Leukocytes are activated during acute inflammation?

A

Phagocytosis using reactive oxygen species ,nitrogen species and lysosomes enzymes.
,Destruction of extra cellular microbes by forming extracellular traps.
Production of chemical mediators to amplify inflammation.

259
Q

What are the differences between phagocytosis and pinocytosis ?

A
Phagocytosis = engulfment of debris, bacteria and other objects. 
Pinocytosis = Engulfment of extracellular fluid.
260
Q

Outline the process of phagocytosis during acute inflammation.

A

The microbe binds to phagocyte receptors and leads to polymerisation of actin in the cells cytoplasms.
The cell cytoplasm then extends to form pseudopods which gradually extend to form a phagocytic vesicle - this pinches off the main cell membrane.
The phagosome produced fuses with a lysosome to create a phagolysosome.
The microbe within the phagolysosome is degraded by hydrolytic lysosomal enzymes.

261
Q

Outline how reactive oxygen species are used to kill microbes in the phagolysosome during acute inflammation.

A

O2 is reduced to become a superoxide anion with the use of phagocyte oxidase present in the phagolysosome membrane.
This superoxide anion then spontaneously dissimilates into hydrogen peroxide before becoming OH-

The OH - is highly destructive to microbes
The H2O2 also combs with myleoperoxidases from within the neutrophil and Cl- to forma hypochlorite which destroys the microbe.

262
Q

How does the polyclonal nature of antibodies affect the amount of antigen dilutions required in the precipitation ring reaction?

A

No effect

263
Q

What type of immunity are the compliment systems part of ?

A

Innate

264
Q

Where are most compliment proteins produced ?

A

The liver

265
Q

How does the classical compliment pathway eventually kill pathogens?

A

It forms a C5b6789 membrane attack complex via a cascade system.

266
Q

How does the alternative compliment pathway eventually kill pathogens?

A

It requires spontaneous hydrolysis of C3 compliment protein. This then triggers a cascade system to produce C5b6789 membrane attack complex.

267
Q

What triggers the alternative compliment system?

A
Bacteria endotoxins (lipopolysaccharides in the outer membrane of bacteria). 
Yeast cell walls.
268
Q

What does the lectin mannose compliment pathway require to continue?

A

Requires mannose binding lectin protein

269
Q

Where is mannose binding lectin protein produced?

A

The liver

270
Q

How is the lectin mannose compliment pathway triggered?

A

When molecules of excess mannose or glucose are present in the body, MASP protease is activated. This then triggers a compliment system producing a membrane attack complex.

271
Q

What are the immune effects of compliment products?

A

Opsonisation
Cell lysis
Chemotaxis
Mass cell production

272
Q

How do compliment systems cause opsonisation?

A

C3b activates neutrophils and macrophages to engulf the invading pathogen by phagocytosis.

273
Q

How do compliment systems cause cell lysis?

A

They produce membrane attack complexes which rupture (bacterial) cell walls.

274
Q

How do compliment systems allow chemotaxis and how is this helpful?

A

C5a attracts neutrophils and macrophages to the invading antigen for phagocytosis.

275
Q

How do compliment systems enable mast cell production and how is this helpful?

A

Some compliment protists activate make cells and basophils which mediate inflammation.

276
Q

What causes immunological memory?

A

Long-lived antibodies
Memory T and B cells
Affinity maturation

277
Q

How do Memory T and B cells cause immunological memory?

A

They last years/decades. Upon re-exposure to the same antigen a greater, faster, more long-lasting secondary response occurs.

278
Q

What is affinity maturation in terms of immunological memory?

A

Produces antibodies which have a greater affinity to the antigen and therefore aids the immunological response.

279
Q

Give an example of a process which allow affinity maturation of antibodies

A

The antibodies may undergo a ‘class switch’ which allows the antibodies to have a greater affinity to the antigen.

280
Q

How do bacteria which attach to host cells evade the defence systems of their host cell ? And what evasion type do the host cells do against this type of bacteria?

A

Host cells block themselves using secretory IgA antibodies. However bacteria contain proteases that split IgA dimers.

281
Q

How do bacteria which proliferate host cells evade the defence system of the host cell? And what type of evasion do the host cells do against this type of bacteria?

A

Host defence system does phagocytosis of bacteria.
However, the bacteria have surface phagocytosis inhibitors and are often able to survive in within the phagocyte if they are engulfed. Bacteria also cause the induction of apoptosis in macrophages to prevent phagocytosis.

282
Q

How do bacterial cells evade the process of compliment-mediated lysis?

A

Gram-positive bacteria don’t allow compliment proteins to bind to their surface and therefore prevent the compliment system attacking them.
They also prevent membrane attack complexed forming by inserting long side chains which interfere with compliment proteins and therefore prevent the compliment cascade.

283
Q

How do bacterial cells which invade host tissues evade the host defence system? And what host defence system is used against this type of bacteria?

A

Ab-mediated agglutination is used by the host cells however, bacteria secrete elastase which inactivates agglutination and they already release hyaluronidase which enhances invasiveness.

284
Q

How does the humeral immune response prevent viruses harming the host?

A

Antibodies prevent fusion of the viral envelope to the cell membrane. They aid opsonisation. They cause agglutination of the virus, making it easier to phagocytose.

285
Q

How do complement systems prevent damage to the host by viruses?

A

Complement systems assist opsonisation and produce membrane-attack complexes which help to kill host cells infected with the virus.

286
Q

Can membrane attack complexes directly kill viruses?

A

No they must produce a membrane attack complex which helps kill the virus.

287
Q

How does the immune system use gamma interferons to prevent damage by viruses? What type of immune response is this?

A

Cell-mediated response.

Gamma interferons act as a direct antiviral agent to stop virally infecting cells replicating.

288
Q

How does the immune system use cytotoxic T cells, NK cells and macrophages to prevent damage to the host by viruses?
What type of immune response is this?

A

They cells kill cells which have been infected with the virus.
Cell mediated response

289
Q

How do some viruses prevent the complement cascades?

A

They bind to complement components and therefore prevent the compliment cascade.

290
Q

How do viruses cause antigenic drift?

A

Point mutations in genes coding for immunogenic glycoproteins on the surface of the virus. Glycoproteins on the surface of the virus change structure meaning antibodies that were produced are no longer complimentary. This means the virus mutates and avoids being affected by the immune system?

291
Q

How is antigenic drift beneficial to viruses?

A

The glycoprotein on the surface of the virus change structure meaning they are no longer complimentary to the antibodies which have been produced by the immune system. This means the virus mutates and avoids been affected by the immune system.

292
Q

How do viruses cause antigenic shift?

A

Antigens on the surface of the virus are completely altered by a combination of genomes. This means the secondary immune response isn’t possible.

293
Q

What methods do parasites use to evade the immune system?

A

They do antigenic drift whilst in host cells to disguise themselves.
They can disguise as host cells by eating themselves with host glycoproteins.
They use trypanosomes to secrete substances with a general suppressive effect on the immune system.

294
Q

What is anaphylaxis?

A

A serious allergic reaction that is rapidly onset and may cause death.

295
Q

What are dimers?

A

2 identical molecules linked together.

296
Q

What are the main functions of the blood?

A

Transports (dissolved gases hormones, nutrients, heat, waste).
Regulation (pH, temperature, absorption, blood flow, osmosis).
Protections (forms clots, transports WBC’s).

297
Q

Describe the viscosity of the blood in comparison with water.

A

More viscous

298
Q

What should the temperature of the blood be?

A

37 digress celcius

299
Q

Describe the pH generally of blood.

A

Slightly alkaline.

300
Q

Describe the colour of the blood when saturated and un-saturated with oxygen.

A
Saturated = Bright red
Un-saturated = Dark red
301
Q

What % of body mass is the blood?

A

8

302
Q

What hormones regulate blood volume and osmotic pressure?

A

Aldosterone
ADH
Anti-natiuretic peptide

303
Q

What plasma proteins are in the blood? (4)

A

Albumins
Globulins
Fibrinogens
Regulatory proteins

304
Q

What do albumin plasma proteins do?

A

Control blood osmolarity

305
Q

What do globulin plasma proteins do?

A

Transport ions, hormones, lipids and have immune functions.

306
Q

What do fibrinogen blood proteins do?

A

Essential component of the clotting system.

307
Q

What are the purpose of electrolytes in the blood?

A

Aid vital cellular activities and contribute to osmotic pressure of the body

308
Q

What are organic nutrients in the blood used for?

A

The are used for ATP production and growth and maintenance of cells.

309
Q

What are the purpose of anticoagulants in a blood sample?

A

They are used to keep a blood sample in liquid form. If this is not used, the blood cells will sink to the bottom and the plasma will be at the top after centrifugation.

310
Q

What is used to keep a blood sample in liquid form?

A

Anticoagulants

311
Q

What is haematology?

A

A form of healthcare concerned with diagnosing and monitoring diseases of the blood and blood forming organs.

312
Q

What are MHC levels of the blood?

A

They are the average about of haemoglobin in each red blood cell. Uses the average weight of haemoglobin and the volume of red blood cells present.

313
Q

What is erythrocyte sedimentation rate a measure of ?

A

An indirect measure of inflammation

314
Q

How may erythrocyte sedimentation rate alter during inflammation?

A

The number of red blood cells will fall more rapidly than usual.

315
Q

What is coagulation screening used to identify?

A

Bleeding issues with the blood.

316
Q

What are haematinic assays used for?

A

They measure factors involved with red blood cell production to identify issues such as anaemia.

317
Q

What are the medical uses of immunophenotyping?

A

Used to identify haematological malignancies.

Can identify the size and complexity of different cells

318
Q

What are the uses of electrophoresis in terms of the blood?

A

They are used to identify the different types of haemoglobin in a blood cells. Can identify diseases cause by haemoglobin.

319
Q

What technique can be used to identify sickle cell anaemia?

A

Electrophoreis.

320
Q

Which blood components maintain osmotic pressure?

A

Albumins

321
Q

What vacutainer should be used to collect a sample for syphillis analysis?

A

Gold

322
Q

What type of feedback controls red blood cell and platelet count in the blood?

A

Negative.

323
Q

What causes white blood cell numbers in the blood o fluctuate?

A

Infection

324
Q

What is the technical name for the formation of blood cells?

A

Haemopoiesis

325
Q

What is Haemopoiesis?

A

The formation of blood cells

326
Q

Where are red blood cells formed ?

A

Red bone marrow

327
Q

What causes red bone marrow to become yellow?

A

Fatty deposits accumulate over time.

328
Q

What can cause yellow bone marrow to become red again?

A

Trauma

329
Q

Where are plutipotent stem cells found?

A

Red bone marrow

330
Q

How does the bone marrow of patients with leukaemia differ from healthy bone marrow?

A

Leukaemia patients will have large leukaeamic blasts forming.

331
Q

What types of diseases can red bone marrow examination identify?

A

Anaemias, proliferate malignancies, leukaemia, cell morphology changes.

332
Q

What subtypes of stem cells do pluripotent stem cell produce?

A

Myeloid stem cells and lymphoid stem cells

333
Q

Where do myeloid stem cells develop?

A

Red bone marrow

334
Q

What cell types do myeloid stem cells give rise to?

A

Platelets, red blood cells, monocytes neutrophils, eosinophils and basophils.

335
Q

What cell types of lymphoid stem cells give rise to?

A

Lymphocytes.

336
Q

Where do lymphoid stem cels develop and where do they end up?

A

Develop = red bone marrow

End up = lymphatic system

337
Q

What are pluripotent stem cells?

A

Can differentiate into any cell type.

338
Q

What are the purpose of erythropoietin?

A

They make myeloid stem cells differentiate into red blood cells.

339
Q

What makes myeloid cells differentiate into red blood cells?

A

Erythropoietin

340
Q

Where is erythropoietin produced?

A

Kidneys

341
Q

What is the purpose of thromopoeitins?

A

They cause myeloid cells to differentiate into platelets.

342
Q

What causes myeloid cells to differentiate into platelets?

A

Thrombopoietins

343
Q

What is the purpose of the lymphatic fluid?

A

Carries waste products around the body.

Carries cells that are part of the immune system.

344
Q

What takes lymph fluid to the lymph nodes?

A

Lymph vessels

345
Q

What are progenitor cells and what cell type do they derived from?

A

Derive from myeloid stem cells.

Cannot reproduce but form CFU and CFU-E cell types.

346
Q

What are precursor cells and what cell type do they derive from?

A

Precursor cells develop into formed elements of the blood over many divisions.

347
Q

What can CFU cell types be recognised by?

A

Can’t be recognised by microscopy.

Can be recognised in bone marrow biopsies.

348
Q

Why can CFU cells be recognised in bone marrow biopsies?

A

They are large and have a high nuclear/cytoplasm ration.

349
Q

How might kidney failure affect blood cell formation and what are the physiological effects of this?

A

No Erythropoietin will be produced so myeloid stem cells won’t differentiate into red blood cells. This may cause anaemia which has a symptom of fatigue.

350
Q

What is one of the main symptoms of anaemia?

A

Fatigue

351
Q

What will be the consequence of lowered Thrombopoietin production?

A

Fewer myeloid stem cells will differentiate into platelets which may cause issues with blood clotting and lead to excessive, extended periods of bleeding.

352
Q

What is the usual life span of a platelet?

A

5-9 days

353
Q

What are the 3 main stages of Haemostasis ?

A

Vascular spasm
Platelet plug formation
Blood Clotting

354
Q

What are the main purposes of mast cells?

A

Dilate blood vessels.
Releases histamines and Herapins to induce inflammation.
Recruits macrophages and neutrophils.
Often responsible for allergic reactions.

355
Q

Where are mast cells found?

A

Connective tissues

Mucous membranes

356
Q

What are the main purposes of macrophages?

A

Phagocytosis of foreign pathogens.

Stimulates the response of other immune cells

357
Q

What are the main purposes of monocytes?

A

Differentiate into macrophages and dendritic cells in response to inflammation.

358
Q

Where are monocytes found?

A

They are stored in the spleen but move through the blood vessels to the required tissues.

359
Q

What are the main purposes of neutrophils.

A

First responders at the site of infection or trauma.
Release toxins that kill or inhibit bacteria and fungi.
Recruit other cells to the site of infection.

360
Q

What are the main purposes of basophils?

A

Responsible for defence against parasites. Release histamines that cause inflammation and are often responsible for allergic reactions.

361
Q

What are the main purposes of Eosinophils?

A

Release toxins that kill bacteria and parasites but also cause tissue damage.

362
Q

What is the purpose of red blood cells having no nucleus?

A

Saves space for more haemoglobin to be present and therefore the ability to carry more oxygen or carbon dioxide.

363
Q

What is the purpose of the red blood cells having no mitochondria?

A

They don’t use oxygen and only do anaerobic respiration so the oxygen they carry will be transported to other body parts.

364
Q

What is the purpose of Nitric Oxide in the blood?

A

Vasodilation.

Thrombotic control - control of blood clotting. Prevents the blood agglutinating when it shouldn’t.

365
Q

What is thrombotic control?

A

Control of blood clotting.

366
Q

What is the purpose of carbonic anhydrase in red blood cells?

A

Creates carbonic acid which dissociates into bicarbonate ions. These ions act as a buffer for the blood and allow the plasma to carry carbon dioxide.

367
Q

What effect does testosterone have on redd blood cell production and how?

A

Causes Erythropoietin to be produced so more myeloid stem cells differentiate into red blood cells.

368
Q

What is Haematocrit?

A

The ratio of the total volume of red blood cells to the total volume of the blood.

369
Q

What causes Polycythaemia?

A

When too many red blood cells are present in the blood and causes blood viscosity to become too high.

370
Q

What happens when a person has Polycythaemia? (symptoms)

A

Their blood becomes too viscous so the heart must work harder.
Blood pressure increases and therefore there is an increased risk of stroke.
Improper red blood cell production.
Tissue hypoxia.
Dehydration.

371
Q

What is meant by the term ‘hypoxia’ ?

A

Deprived of oxygen

372
Q

What causes neutrophil counts to increase and decrease?

A
\+ = Bacterial infection, stress, burn, inflammation. 
- = Radiatioon exposure
373
Q

What causes lymphocyte counts to increase or decrease?

A
\+ = Viral infection, some Leukaemias. 
- = Prolonged illness, immunosupression
374
Q

What causes monocyte counts to increase or decrease?

A
\+ = Viral or fungi infection, some chronic illnesses. 
- = Bone marrow suppression.
375
Q

What causes Eosinophil count to increase or decrease?

A
\+ = Allergic reactions, parasitic infections. 
- = Toxic drugs, stress
376
Q

What causes Basophil count to increase or decrease?

A
\+ = Allergic reactions, leukaemia, cancer
- = Pregnancy, ovulation, stress
377
Q

How high a suspected cause of Polycythaemia be investigated?

A

Carrying out a red blood cell count. Excessive red blood cells could indicate polycythaemia.

378
Q

How may an elevated basophil count become apparent?

A

Excessive and un-necessary inflammation.

379
Q

On a blood smear lots of cells with lightly stained granules and multi-lobed nuclei are found. What are these likely to be ?

A

Neutrophils or Eosinophils.

380
Q

What is blood doping?

A

A way of improving athletic performance by artificially boosting the blood’s ability to bring more oxygen to the muscles.

381
Q

What do type 1 interferons stimulate the synthesis of?

A

Anti-viral proteins

382
Q

What part of immunity do type 1 interferons belong to?

A

Natural

383
Q

What cell types produce type 1 interferons?

A

Macrophages

384
Q

Is an adaptive immune response capable of memory?

A

Yes

385
Q

Neutrophils secrete a greater variety of substances. than macrophages. True or False?

A

False

386
Q

Do antigenic molecules contain amino acids? and if so, what type?

A

Yes - likely to be aromatic

387
Q

Are antigenic molecules likely to be soluble or insoluble?

A

Insoluble

388
Q

Are antigenic molecules likely to contain simple or complex sugars?

A

Complex

389
Q

What does primary immunodeficiency arise from?

A

Infections

390
Q

Can primary immunodeficiency arise from complement defects?

A

No

391
Q

What is the site of maturation for the lymphocyte subset?

A

Thymus

392
Q

What filters out microorganisms which have been washed up by the lymphatics into the interstitial fluids?

A

Lymph nodes

393
Q

What are the purpose of the lymph nodes?

A

They filter out microorganisms which have been washed up by the lymphatics into the interstitial fluids.

394
Q

After how many hours does acute inflammation peak?

A

24

395
Q

What is the purpose of the spleen in terms of immunology?

A

Is the main lymphoid tissue to protect against blood-born antigens.

396
Q

What is the main lymphoid tissue to protect against blood-born antigens?

A

The spleen

397
Q

How do tonsils aid immunology?

A

Protect against oral and nasal pathogens.

398
Q

What is the purpose of the Mucosa-associated lymphoid tissue? (MALT)

A

Defends the lining of externally opening organs.

399
Q

How does the herpes simplex virus prevent an immune response generally?

A

Inhibits antigen processing

400
Q

How does the vaccinia virus prevent an immune response?

A

Binds to complement components

401
Q

How does Hepatitis virus C prevent an immune response?

A

Blocks interferons

402
Q

How does HIV prevent an immune response?

A

Reduces MHC class II

403
Q

How does adenovirus prevent an immune response?

A

Reduces MHC Class I

404
Q

Does MAC or perforin cause cytolysis?

A

Both

405
Q

How many epitopes do monoclonal antibodies bind to?

A

1

406
Q

What cell type are monoclonal antibodies produced by?

A

A single B cell clone

407
Q

What is the overall purpose of the acute phase response?

A

A means of reducing bacterial toxicity and limiting tissue damage.

408
Q

What is the acute phase response mediated by?

A

Macrophage cytokines.

409
Q

Describe the relative sizes of neutrophils and macrophages.

A

Neutrophils are smaller.

410
Q

Describe the relative lengths which neutrophils and macrophages last in circulation.

A

Macrophages last longer.

411
Q

What chemical is produced when cytotoxic T cells are activated?

A

Perforin

412
Q

What is the purpose of interleukin 2 ?

A

An autocrat stimulator of helper T cells.

413
Q

What type of cells does Costimulation require?

A

Antigen-presenting cells

414
Q

Which MHC class associated antigens do macrophages present?

A

MHC class II

415
Q

What type of cytotoxic T cells does interleukin 2 costimulate?

A

Antigen-bound cytotoxic T cells

416
Q

What type of interferons do activated cytotoxic T cells produce?

A

Gamma interferons

417
Q

When type 1 interferons are stimulated, what type of proteins do they produce?

A

Anti-viral

418
Q

What mediates the acute inflammatory response?

A

Complement

419
Q

Activation of complement results in perforin production - true or false?

A

False

420
Q

What MHC class do endogenous antigens complement with ?

A

MHC class I

421
Q

What cell type are endogenous antigens recognised by?

A

Cytotoxic T cells

422
Q

How do natural killer cells kill pathogens (generally)?

A

Release perforin

423
Q

What cells release histamine?

A

Mast cells

424
Q

In the tethering process of platelet formation, outline the process, what extracellular matrix protein is required and the receptor needed.

A

Platelet binds to exposed extracellular matrix and therefore stops moving.

This requires vWF which is stuck on collagen.

Receptor: GpIb/v/IX

425
Q

In the activation process of platelet formation, outline the process, what extracellular matrix protein is needed, what receptor is needed.

A

Platelets release granule content, spread and adhesion receptors are activated.

ECM collagen needs.

Receptor: GPVI

426
Q

In the adhesion process of platelet formation, outline the process, what extracellular matrix protein is needed and what receptor is needed.

A

Single layer of platelet binds to the extracellular matrix.

Collagen

Receptor: a2B1

427
Q

In the secretion process of platelet formation, what happens?

A

Platelets release the platelet activating chemicals ADP and TxA2.

428
Q

In the aggregation process of platelet formation, what happens, what extracellular matrix proteins is required and what receptor is required?

A

Multiple layers of platelets bind to each other.

Fibrinogen required

Receptor: aIIbB3

429
Q

What are the 3 main types of haematological malignancies?

A

Common Leukaemias.
Myeloproliferate Neoplasms.
Multiple Myeloma.

430
Q

What are Leukaemias?

A

The presence of malignant Leukocytes within the peripheral blood or bone marrow. Therefore suppressing production of all normal cells in the red bone marrow.

431
Q

What is meant by the term ‘malignant’ in terms of cells?

A

Cells that divide without control.

432
Q

What are Lymphomas?

A

Cancers with a lymphoid origin.

433
Q

What are some symptoms of Leukaemia?

A

Weight loss, shortness of breath, weakness, pain of joints and bones, fatigue, loss of appetite, swelling, enlargement of the liver and spleen, easy bleeding and bruising, purple patches or spots on the skin.

434
Q

Why does Leukaemia cause swelling of the lymph nodes, spleen and liver.

A

These areas will overcompensate and try to make excess red blood cells when tumours are present.

435
Q

What characterises acute Leukaemia?

A

Immature immune blast cells make up at least 20% of the nucleated cells in the bone marrow.

436
Q

Other than high blast count in the bone marrow, what else can indicate acute Leukaemia?

A

Evidence of arrest of immune cell maturation.

437
Q

Is chronic or acute Leukaemia more aggressive?

A

Acute

438
Q

What characterises chronic Leukaemia?

A

Have less than 20% of immature blast cells making up their nucleated cells in the bone marrow.

439
Q

Why do malignant cells accumulate in chronic inflammation?

A

Cells don’t do apoptosis

440
Q

Does maturation arrest of immune cells occur in acute or chronic Leukaemia?

A

Acute

441
Q

What are the 2 main derivatives of Leukaemia?

A

Myeloid

Lymphoid

442
Q

What is meant by a Leukaemia being myeloid?

A

Arising from neutrophil, monocyte, basophil or eosinophil pre-crusor cells.

443
Q

What is meant by a Leukaemia being lymphoid?

A

Arising from B-lineage or T-lineage lymphocytes, Natural killer cells or their pre-cursors.

444
Q

What are the 4 overall types of Leukaemia?

A

Acute lymphoblastic Leukaemia.
Chromic lymphocytic Leukaemia.
Chronic Myelogenous Leukaemia.
Acute Myelogenous Leukaemia.

445
Q

In what people is Acute Lymphoblastic Leukaemia most common ?

A

Children

446
Q

What is the onset relative time of acute lymphoblastic leukaemia?

A

Short onset

447
Q

In what people is Chromic lymphocytic Leukaemia most common?

A

Adults 55+

448
Q

What people does Acute myelogenous Leukaemia affect most?

A

All ages

449
Q

Describe the relative onset time of chronic myelogenous Leukaemia.

A

Long onset time

450
Q

What type of people does Chronic myelogeonous Leukaemia mostly occur in?

A

Adults

451
Q

Why do cancer cells produce excessive white blood cells?

A

Cancer cell mutations (oncogenes) are acquired in the stem cells. Stem cell maturation is then dysregulated and excessive numbers of white blood cells are produced.

452
Q

What are the risk factors and possible causes of Leukaemia?

A

Radiation exposure, smoking, genetic disorders, benzene.

453
Q

Why are people who have previously had cancer more likely to get a different type of cancer ?

A

Cancer treatments can be a risk to causing other tumours of different types.

454
Q

What are the causes of Acute lymphocytic leukaemia?

A

Chromosomal mutations resulting in abnormal transcription factors that affect the development of B and T cells.

455
Q

What are the cells involved in acute lymphocytic Leukaemia?

A

Immature T and B cells.

456
Q

What are the causes of Chromic Lymphocytic Leukaemia?

A

Chromosomal deletion or point mutations of the B cells.

457
Q

What cell types does Chronic Lymphocytic Leukaemia affect?

A

Peripheral T and B cells in the lymph nodes

458
Q

Explain the difference of how common Chronic Lymphocytic Leukaemia is in women and men.

A

Twice as common in men.

459
Q

What are the causes of Acute Myelogenous Leukaemia?

A

Onocgenic mutations impede differentiation meaning that immature myeloid blasts accumulate in the bone marrow.

460
Q

What are the common symptoms of Acute Myelogenous Leukaemia?

A

Anaemia, Spontaneous bleeding.

461
Q

What are the causes of Chronic Myeloid Leukaemia?

A

Thyrosine kinase pathway related chromosomal translocation - Philadelphia chromosome.

462
Q

What cells are affected in chronic myeloid leukaemia?

A

Pluriptotent hematopoetic stem cells.

463
Q

What are the common symptoms of chronic myeloid leukaemia?

A

Slow onset, mild anaemic symptoms.

464
Q

What are the common symptoms of acute lymphocytic Leukaemia?

A

Fast onset, depressed bone marrow function, bone pain

465
Q

What are the common symptoms of chronic lymphocytic leukaemia?

A

Asymptomatic or non-specific symptoms

466
Q

What is the Philadelphia chromosome and how does it cause Leukaemia?

A

The gene ABL1 on chromosome 9 gets stuck to the gene BCR on chromosome 22. This creates a mutation (BCR-ABL1).
This mutation codes for thyroxine kinase, which causes myeloid white blood cell production and but stops these cells from developing into normal blood cells or dying.

These abnormal cells are Leukaemia cells.

467
Q

On what chromosome is the ABL1 gene?

A

9

468
Q

on what chromosome is the BCR gene?

A

22

469
Q

What are bone marrow transplants used for?

A

To replace cancerous red bone marrow with healthy red bone marrow.

470
Q

What medication must a patient be taking during a bone marrow transplant?

A

The patient must stay on immunosuppressants.

471
Q

What methods are used to destroy unhealthy red bone marrow in a bone marrow transplant?

A

Chemotherapy or whole body radiation.

472
Q

What is Leukaemia?

A

The presence of malignant Leukocytes within the blood or bone marrow that suppress the production of other cells.

473
Q

What are Myeloproliferate Neoplasms in general?

A

A group of rare disorders of the bone marrow that cause in increase in the number of blood cells produced

474
Q

How many different types of blood cell are produced in excess when a person has myeloproliferate neoplasms?

A

1 or more

475
Q

What are myfibroblasts?

A

Cells that synthesise collagen for the extra-cellular matrix.

476
Q

What (in general) is Thrombocythemia?

A

A blood disorder that causes an extremely high number of platelets to be produced.

477
Q

Why do people experience abrnomal bleeding if they have thrombocythemia?

A

Platelets produced are not maturing properly so don’t function effectively.

478
Q

What causes patients with thrombocythmia to experience dizziness, headaches, fainting etc?

A

Blood clots forming in several organs of the body.

479
Q

What causes patients with thrombocythemia to experience ministrokes?

A

Blood clots in arteries that supply the brain.

480
Q

What is the main cause of Polycythemia Vera?

A

JAK2 mutation

481
Q

What is Polycythemia Vera (overview)?

A

Slow-growing blood cancer where the bone marrow produces too many red blood cells.

482
Q

Why do people with Polycythemia Vera have low levels of EPO?

A

This is caused by a negative feedback system.
The body knows it is producing excessive amounts of red blood cells so stops producing EPO. However, the excessive red blood cell production is irrelevant of EPO concentration so this effect has no change.

483
Q

What mechanism does the JAK2 mutation in patients with Polycythemia Vera affect?

A

It affects the Thyrosie Kinase receptor signalling pathway and causes cells to proliferate un-necessarily.

484
Q

How would the blood film of an individual with Thrombocythemia be different than a normal blood film?

A

Aggregations would occur - clotting would show.

More platelets would be visible.

485
Q

What is Myelofibrosis in general?

A

A rare condition affecting the bone marrow. Scar tissue builds up inside the bone marrow meaning that blood cells aren’t made properly.

486
Q

Why do the spleen and liver become enlarged in patients with Myelofibrosis?

A

The liver and spleen try to compensate for the lack of blood cells being produced by the bone marrow.

487
Q

What is primary Myelofibrosis?

A

People who haven no history of problems with their bone marrow getting myelofibrosis.

488
Q

What is secondary myelofibrosis?

A

Where primary myelofibrosis developes in people who already have issues with their bone marrow.

489
Q

What type of Leukaemia is sometimes acquired by individuals with myelofibrosis?

A

Acue Myeloid Leukaemia

490
Q

What causes thick, coarse fibres to to form in the bone marrow during Myelofibrosis?

A

Increased expression of inflammatory cytokines from mutated megakaryocytes and other platelet forming cells.

491
Q

What replaces the bone marrow over time when a patent has Myelofibrosis?

A

Thick coarse fibres

492
Q

What happens to the production of blood cells over time when a patient has Myeloifibrosis and why?

A

Coarse fibres replace the bone marrow meaning fewer number of blood cells are produced. This results in anaemia.

493
Q

what are some of the symptoms of Myelofibrosis?

A

Fatigue, bone pain, night swears, fever.

494
Q

What are pulmonary embolisms?

A

A blood clot that occurs in the lungs and can damage areas of the lungs due to restricting blood flow and therefore decreasing oxygen delivery.

495
Q

What is cytopenia?

A

A reduction in the number of mature blood cells.

496
Q

What cells does multiple myeloma affect?

A

Plasma cells of the bone marrow.

497
Q

What environmental risk factors are associated with multiple myeloma?

A

Herbicides, insecticides, benzene, hair dyes and radiation

498
Q

What is the cause of multiple myeloma?

A

Plasma cells undergo malignant transformation and stop making different forms of antibodies and instead start to produce a single, abnormal type of monoclonal antibody.

Multiple myeloma plasma cells accumulate in the bone marrow and erode the hard-outer shell that usually surrounds the marrow.

499
Q

What are the symptoms of multiple myeloma?

A

Weakened bones, easily broken and fractured bones, anaemia.

500
Q

What is osteoporosis?

A

Bone thinning and weakening

501
Q

What causes thickened blood in people with multiple myeloma?

A

Vast production of ‘M protein’.

502
Q

What methods are used to treat multiple myeloma?

A

Chemotherapy drugs, radiation therapy, stem cell transplants and taking drugs that modulate the immune system.

503
Q

What is cell morphology ?

A

The specific phenotype of a cell ; shape, structure, form and size.

504
Q

What are haematological malignancies?

A

Cancers that begin in the cells which are then subdivided according to the type of blood being affected.

505
Q

What are MHC levels?

A

The average haemoglobin in each red blood cell.

506
Q

What are MHCH levels?

A

The average weight of haemoglobin present based on the volume of red blood cells.

507
Q

What is cytometry?

A

Determining the size, shape and nucleic acid content of cells using a flow cut-meter.

508
Q

What is a blood film used to identify?

A

Altered numbers and staining to diagnose diseases such as anaemia and leukaemia.

Morphology changes that indicate genetic disorders.

509
Q

What Can a full blood count identify?

A

No of cells of each type.
MHC levels.
MHCH levels.

Therefore altered functioning or presence of red blood cells and haemoglobin.

510
Q

What do erythrocyte sedimentation rate experiments identify and what does this help identify?

A

Measures the mm of clear blood plasma in the top of a column after one hour. Indirectly measures inflammation.

511
Q

What does a coagulation screen identify?

A

Identifies if bleeds are due to deficiencies in the common, intrinsic or extrinsic coagulation pathways.

512
Q

What are haematological assays and what can they identify?

A

Measures factors that are involved with control of red blood cell production.

Used to investigate treatments for anaemia.

513
Q

What is immunophenotyping?

A

Using flow cytometry to analyse proteins on the surface of white blood cells.

514
Q

What is immunophenotyping used to identify?

A

Haematological malignancies.

515
Q

What can be identifies using haemoglobin variation detection by gel electrophoresis?

A

Analyses malignant cell types and identifies sickle traits.

516
Q

How does nitric oxide affect platelet adhesion?

A

Reduces it

517
Q

Which type of leukaemia is the Philadelphia chromosome associated with?

A

Chronic myeloid leukaemia

518
Q

Which type of leukaemia is essential thrombocythemia associated with?

A

Chronic myeloid neoplasms

519
Q

What is the main feature of essential thrombocythemia?

A

Excess platelets