General Flashcards
(519 cards)
1
Q
What is Apostasis?
A
Removing cells that have died of natural causes
2
Q
When does Apostasis normally occur?
A
Embryonic development and ageing
3
Q
What is the main overall purpose of Apostasis?
A
Maintain cell populations within tissues.
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
5
Q
What is innate immunity?
A
Non-specific - natural immune system
6
Q
What type of immunity does the skin cause and how does it do this?
A
Innate immunity. Protects underlying tissues from microbes.
7
Q
What is the technical name for sweat glands and what are their purpose?
A
Sudoriferous (sweat) hands produce lysosomes that degrade peptidoglycands.
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.
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.
10
Q
Name a type of non-pathogenic bacteria that surpasses virulent bacteria.
A
Commensal bacteria. Non-pathogenic bacteria.
11
Q
Where is commensal bacteria found - examples.
A
Skin, mouth, reproductive regions, gastrointestinal tracts.
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.
13
Q
What antibacterial substances do commensal bacteria release?
A
Colicins-proteins, short fatty acids.
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.
15
Q
How do hairs in the nose act as a type of innate immunity?
A
Increase surface area and therefore increase trapping potential.
16
Q
Name types of innate immunity (general).
A
Mucous membranes, hairs, acid, flushing, commensal bacteria, skin, eyes, ears, mouth.
17
Q
What is secreted from the ears as part of innate immunity?
A
Cerumen waxy secretion from the sebaceous glands.
18
Q
What is produced by a humoural immune response?
A
Antibodies
19
Q
What is produced by a cell-mediated immune response?
A
Cytotoxic T lymphocytes.
20
Q
Where does Hematopoiesis occur?
A
The hematopoietic system (bone marrow, liver, spleen etc.)
21
Q
When does Hematopoiesis begin?
A
Embryonic development.
22
Q
What (in general) is hematopoiesis?
A
Replacing old red blood cells with new red blood cells.
23
Q
Name the 2 main categories of phagocytic cells
A
Granulocytes and Macrophages
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.
25
Name two types of macrophages and any further details.
Wandering macrophages- travel as monocytes around the body, do chemotaxis during inflammation.
Fixed Macrophages- Present in most organs.
26
What are the 2 ways that a phagocyte attaches to a bacterium?
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.
27
What is a Phagolysosome?
A digestive vesicle formed within a cell by the fusion of a phagaosome containing ingested material and a lysosome containing hydrolytic enzymes.
28
What are the 2 killing mechanisms of Phagoytosis?
Oxygen-dependent and Oxygen-independent
29
What happens during oxygen-dependent killing mechanisms of phagocytosis?
Lysosomes degrade bacterial cell walls, cationic proteins cause pH to fall, defensives bind to bacterial membranes and form pores, acid hydrolase enzymes degrade carbohydrates.
30
What are the 3 ways that Apoptosis can occur?
Intrinsic pathway
Extrinsic pathway
Apoptosis Inducing Factor
31
Describe the intrinsic apoptosis pathway.
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.
32
Describe the extrinsic apoptosis pathway.
Death receptors (integral membrane proteins) bind to death activating molecules outside the cell. Caspase 8 activated inside cell. Destroys organelles.
33
How does the Apoptosis inducing factor theory work?
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
34
Where is apoptosis inducing factor found ?
Intermembrane space between the inner and outer mitochondrial membranes.
35
How do macrophages generally work in terms of B cells?
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.
36
Where are B lymphocytes produced?
Bone marrow
37
Where can an example of humoural immunity be found?
In Macrophages.
38
Where are T lymphocytes produced and matured?
Produced- Bone marrow
| Matured- Thymus
39
What happens to T-lymphocytes when the body is infected and how does cell mediated immunity then occur?
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.
40
Where does Hematopoeisis occur?
Bone marrow
41
What type of cells to Haematopoeitic stem cells differentiate into?
Myeloid cell types or Lymphoid cell types.
42
What types of Lymphoid cells are present in Haematopoeisis?
T lymphocytes and B lymphocytes
43
Name a type of Myeloid cell
Erythrocyte, Megakaryocyte, Monocyte, Neutrophil, Basophil, Eosinophil.
44
What type of cell is a Megakaryocyte and what is its function?
Myeloid cell - gives off cytoplasm to form platelets.
45
Describe the naming difference in T and B cells before and after they have matured.
Immature- B Lymphoblasts and T Lymphoblasts.
| Mature - B Lymphocytes and T Lymphocytes.
46
What are dendritic cells and where are they found?
A type of immune cell found in the sin, gut, lungs, digestive tract etc.
47
Explain in general how an enzyme- cascade system works and what it is.
An in-active enzyme is activated. This newly activated enzyme then activates another enzyme and the cycle continues.
The initial effect is amplified.
48
What are 4 major cascade systems in the blood?
Blood clotting
Kinin
Firbrinolytic
Complement
49
Draw a flow diagram showing how the alternative complement system causes immunity based on C3.
IN NOTES !!!
50
What are the 3 general outcomes of the alternative complement pathway.
Cytolysis, phagocytosis, inflammation.
51
Give an example Opsonisation and its benefits.
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.
52
Where are most complement enzymes before activation?
In the blood as pre-enzymes.
53
What is the general onset time and duration of chronic inflammation?
Slow onset, long duration
54
What is the general onset time and duration of acute inflammation?
Rapid onset, short duration
55
What are the 3 pathways of the complement system?
Alternative, Classical, Lectin
56
What usually causes acute inflammation ?
Microbes, chemical irritants, physical trauma, exposure to extreme temperature.
57
What cell type is used to combat acute inflammation ?
Neutrophils
58
Where are neutrophils activated during the acute inflammation process?
In the endothelium cells lining blood vessels.
59
What are the features of activated neutrophils in the acute inflammation system?
Increased receptors for chemoattractants, prostaglandins , leukotrienes and FCs. As well as more complement proteins.
60
How does activation of neutrophils affect metabolic activity and hows this helpful for immunity.
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.
61
Outline to sequence of events in acute inflammation.
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
62
How are prostaglandins and Leukotrienes stored ?
They cannot be stored so must be made from scratch during the acute inflammation process.
63
What is oedema?
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.
64
What tissue damage can occur due to acute inflammation?
Tissue damage can occur but is usually very minor and impermanent.
65
What systems are in place to limit the tissue damage during acute inflammation?
Chemicals such as TGF beta stop and slow the inflammatory response.
66
What repairs are made after acute inflammation damage?
Fibroblasts are stimulated to repair the extra-cellular matrix for cells and produce collagen to repair tissue.
67
What are the symptoms of the inflammation (Latin name and explanation ).
```
Calor - heat
Dolor - Pain
Rubor - Redness
Tumour - Swelling
Functio Laesa - loss of function
```
68
What is extravasation in general terms?
How neutrophils move from the blood vessels to the site of damage.
69
What is the purpose of the vascular endothelium in cells?
Acts as a gateway regulating movement of molecules between cells and the blood.
70
What type of molecules are vital for Extravasation?
Cell adhesion molecules (CAMs).
71
Explain the process of Extravasation and how it allows neutrophils to reach the invaded site.
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.
72
What are interferons (general)?
Proteins produced by certain types of cells infected with viruses.
73
What is the main function of interferons and are they specific?
Non-specific
| Interferons inhibit viral replication.
74
What are the functions of type 1 interferons and what are the type 1 interferons?
Alpha and beta interferons. Suppress tumours and metastasis.
| Used to trat Kaposi's sarcoma, genital warts and hepatitis C.
75
What is metastasis?
Abit of tumour splits off and goes to another part of the body to use a secondary tumour.
76
What are the type 2 interferons and what are their functions?
Gamma interferons.
| Activates neutrophil and macrophages to enhance phagocytosis and the inflammatory process.
77
What cell types are the 2 interferons secreted from?
Natural killer cells and cytotoxic T cells.
78
How do interferons work to inhibit viral replication?
Interferons diffuse into neighbouring cells and bind to surface receptors. Interferons stimulate tissue cells to synthesise anti-viral proteins that inhibit viral replication.
79
By what method do natural killer cells kill cells?
Cytolysis and they also induce apoptosis.
80
What cells differentiate into natural killer cells?
Common lymphoid progenitor cells - innate lymphoid cells - natural killer cells.
81
Where are natural killer cells found?
Lymph nodes, spleen, bone marrow, blood.
82
Why are natural killer cells so fast acting and powerful?
They produce and respond to the stimulus to create a magnifying effect.
83
How do natural killer cells cause cytolysis?
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.
84
What types of cell are defensives active against?
Bacteria, fungi and some viruses.
85
How do defensives kill off pathogens?
They form pores in target cells and therefore affect osmotic potential - leading to osmotic lysis.
86
What are cells are pattern recognition receptors on and what pattern types do they recognise?
Proteins on innate immune cells and epithelial cells.
| They recognise pathogen-associated molecular patterns and damage-associated molecular patterns.
87
What is the purpose of patter recognition receptors in the inflammatory process?
These proteins bind to pathogens and release inflammatory cytokines.
88
What response accompanies the acute phase response?
The local inflammatory response.
89
What happens during the acute phase response?
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.
90
What stimulates the release the release of acute phase serum proteins?
Cytokines and macrophages.
91
Where are acute phase serum proteins made?
The liver
92
What is the purpose/ function of acute phase serum proteins?
They limit the release and toxicity of bacteria by binding to bacterial phospholipids, activating complementing bacteria and therefore enhancing phagocytosis.
93
What are the effects of the acute phase response ?
Increased body temperature (not ideal for pathogens), ACTH (hormone released which causes cytosol to be made and activate the white blood cells).
94
Where is ACTH hormone made and released?
```
Made = pituitary gland
Released = adrenal glands
```
95
What is the effects of ACTH being released into the adrenal glands?
Activates which blood cells.
96
What are the 2 mechanisms for specific immunity?
Humoral immunity
| Cell mediated immunity
97
What does the specificity of humoral immunity rely on?
Antibodies
98
What does the specificity of cell mediated immunity rely on?
T cells
99
Define antigen .
Any substance that when introduced to the body, is recognised as foreign and is capable of inducing a specific immune response .
100
Define immunogenicity .
The ability to induce an immune response .
101
What is produced when a B cell comes into contact with an immunogen?
Effector B lymphocytes and Memory B cells .
102
What is produced when T cells come into contact with an immunogen?
Effector T lymphocytes and T memory cells are produced .
103
Is an immunogen always an antigen?
Yes
104
Is an antigen always an immunogen?
No
105
What factors is immuogenicity determined by?
Degree of foreigness, molecular size, chemical composition and heterogeneity, susceptibility to antigen processing and presentation .
106
How does degree of foreigness affect immunogenicity?
The more foreign the microbe is and the less similar it is to body cells, the more likely to trigger an immune response .
107
How does phylogenetic evolution affect immunogenicity of a microbe?
As phylogenetic distance increases, the more likely the foreign body is to cause an immune response as it appears less like a self component .
108
Why do some self-components trigger an auto immune response?
Some self-components are sequestered (hidden) so may be recognised as foreign if they enter other regions of the body .
109
How does molecular size affect immunogenicity?
The larger the immunogen, the larger the immune response .
110
How do aromatic amino acids affect immunogenicity?
Increase immunogenicity .
111
What type of stereo-isomers are non-immunogenic?
D isomers because they cannot be degraded .
112
How does solubility increase immunogenicity?
The more insoluble a microbe, the more it aids phagocytosis and therefore the more it aids immunogenicity .
113
What varies the effects of the immunogen on an individual
The genotype of the recipient, immunogen dosage, imunogen route, adjuvants .
114
What are adjuvants in terms of immunogens ?
They work with the immunogen to enhance receptors .
115
Define Atnigenicity .
The ability to combine with products of the immune response .
116
What are endogenous antigens and what cells are they recognised by?
Recognised by Cytotoxic T cells .
| Originate inside the body and presents antigens on its surface .
117
What are exogenous antigens?
Originate outside the body and are recognised by T helper cells .
118
Give an example of an exogenous microbe .
Bacterial infections .
119
What receptors do B lymphocytes have to recognise antigens?
Have B cell antibodies on their surface which act as antigen receptors .
120
What receptors do T lymphocytes have on their surface to recognise antigens?
T cell antigen receptors .
121
What is the advantage of having large antigens?
The larger the antigen the larger the binding site for T/B lymphocytes .
122
Which polysaccharides do/ don't trigger an immune response?
Small dont
| Large do
123
What are epitopes?
The site on an antigen molecule where the antibody binds .
124
How many epitopes sites can an antibody bind to?
1 - they are highly specific .
125
How many epitopes do antigens have on their surface and why?
Many because this allows the effective production of many different antibody types to allow an effective immune response .
126
What are haptens?
Molcules which are too small to initiate an immune response .
127
How can haptens be made to cause an immune response?
Haptens can be linked to carrier molecules to trigger an immune response and react with an antibody .
128
Are haptens antigenic and immunogenic when linked with a carrier molecule?
They are antigenic but not immunogenic .
129
Define antibodies .
A group of protein globuin glycoproteins and immunoglobulins present in the blood plasma that combine with the antigenic determinant that triggered its prodicton .
130
When is the constant region for the antibodies structure the same?
The same for antibodies of the same class .
131
How many and what type of chains is the antibody structure composed of ?
2 identical inside heavy chains and 2 identical outside light chains .
132
How are the chains of the antibody structure held together?
The 2 heavy chains and held by 2 disulphide bridges . The heavy chains are attached to the light chains by 1 disulphide bridge .
133
What causes the Y shape of he antibodies .
Hinge regions on the heavy chains which enable flexibility .
134
What are variable regions of the antibody structure?
Tips of the heavy and light chains which act as antigen binding sites .
135
What are hypervariable regions of the antibody structure?
Very tip of the light and heavy chains .
136
How many hypervariable regions do most antibodies have?
2
137
What is a unique feature of the IgG antibody?
The only antibody that can cross the placenta .
138
What is the purpose and main function of IgG antibodies?
Protect us against bacteria and viruses - high affinity to microbes at epitope sites and trigger complement system, enhance phagocytosis and neutralise toxins .
139
Wha is the general function of IgA antibodies?
Provides localised protection mucus membranes .
140
What is the general function of IgM anitbodies?
Causes lysis of microbes and helps agglutinated of red blood cells .
141
In what ways do antigen-antibody complexes neutralise or eliminate antigens?
Activation of complement systems by the classical pathway, phagocytosis through oposonisation, neutralisation by cross-linking molecules of toxins or viruses .
142
How are monoclonal antibodies made?
Antibody-producing B cells fuse with myeloma cells . This creates a hybridoma which is immortalised and antibody producing .
143
How are monoclonal antibodies used to find cancers?
Toxins are often placed on the tail of monoclonal antibodies and the toxins are then delivered directly to the cancer .
144
What causes the precipitation to occur in the precipitation ring practical?
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.
145
What must be a feature for the precipitate to form in the precipitation ring practical?
The antigens and antibodies must be present in the same concentration.
146
Why is it necessary to use a series of antigen dilutions in the precipitation ring practical?
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.
147
What factors does the forming of a precipitate depend on in the precipitate ring practical?
The affinity of the antigen to the antibody - higher affinity = greater precipitate.
Ratio of antibody to antigen - must be in equal concentrations.
148
Why may no precipitate be present in the precipitate ring reaction?
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.
149
Define precipitin.
Soluble antibodies which react with soluble antigens to form a precipitate.
150
Define Precipitinogen.
Soluble antigens which induce the formation of precipitin.
151
Define lattice in terms of the precipitin ring practical.
The cross linking of antigens and antibodies to form and immunocomplex.
152
What is the equivalence zone in the precipitate ring reaction?
The zone where the concentration of antibodies and antigens is equal. A immunocomplex lattice can form. Precipitate is present.
153
What is the basic difference between Geel diffusion occurring in Oudin tubes and Ouchterlony plates?
Oudin tubes used single, one directional diffusion.
| Ouchterlony plates use 2D diffusion.
154
What is the clinical significance of febrile antibodies?
Used to diagnose infections and diseases such as haemolytic anaemia.
155
Why does Agar jelly resist contamination with bacteria?
Agar is a polymer made up of subunits of galactose and red algae so cannot be easily degraded by micro-organisms.
156
What are semi-quantitative results?
E.g "Less than 5" "Between 5 and 20" "Greater than 20".
157
Which method (Ouchterlony or Precipitation ring reaction) produces a more stable precipitate?
Ouchterlony
158
Are Ouchterlony or precipitation ring reactions quicker?
Precipitation
159
How does agglutination differ from precipitation reactions?
An insoluble antigen is used in agglutination whereas precipitation methods use soluble antigens.
160
Do precipitation methods use soluble or insoluble antigens and antibodies?
Both are soluble but form an insoluble complex.
161
Define inflammation (acute).
The local response of living tissue to any infectious agent.
162
Compare the onset times of acute and chronic inflammation.
Acute - rapid
| Chronic - slow
163
Compare the cells used for acute and chronic inflammation.
```
Acute = Neutrophils
Chronic = Lymphocytes, Monocytes and macrophages.
```
164
Compare the type of tissue injury which induces acute and chronic inflammation.
```
Acute = Mild
Chronic = Severe and processingly worsening
```
165
What are the 5R's / 5 steps to an inflammatory response?
Recognition (of the injurious agent)
Recruitment ( of inflammatory cells - leukocytes)
Removal (of the injurious agent)
Regulation (of the inflammatory response)
Resolution / repair
166
What are the two main overall processes that occur as part of acute inflammation?
Vascular changes
| Cellular events
167
What are the vascular changes that occur during acute inflammation?
Vasodilation and increased vascular permeability.
168
How is vasodilation caused during acute inflammation?
Histamine hormone is used to expand the arterioles and increase the blood flow. This causes the tissue to become red and warm.
169
What process in acute inflammation causes the red and hot symptoms?
Vasodilation
170
What are the overall purposes of vasodilation and increased vascular permeability in acute inflammation?
The blood becomes more viscous so blood flow is slowed. This leaves time for the engorgement of small vessels.
171
What are the 4 ways that vascular permeability increases during acute inflammation?
Explain each one.
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.
172
Explain how transcytosis can cause vascular permeability to increase.
There is increased transport of fluids and proteins into the intracellular channels. The channels are stimulated by vascular endothelial growth factors which promote leakage.
173
What are leukocytes?
A type of white blood cell. Often used in the inflammatory response.
174
What cellular events occur to cause acute inflammation?
Recruitment of Leukocytes.
| Activation of Leukocytes leading to the process of destruction of invading cells and production of mediators.
175
What are the stimuli for acute inflammation.
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
176
What is tissue necrosis?
The passive breakdown of order structure and functions of a tissue resulting in irreversible damage.
177
How are acute inflammation stimuli recognised by the host in general terms ?
They are recognised by receptor on antigen presenting cells and epithelial cells.
178
What 2 types of receptors recognise acute inflammation stimuli?
Toll like receptors
| Inflammasomes
179
What do toll like receptors detect as part of the acute inflammatory response?
They detect microbial stimuli and pathogen products.
180
Where are toll like receptors present?
Plasma membrane and endosomes
181
What are endosomes?
Membrane bound vesicles.
182
What is the outcome of the use of toll like receptors in acute inflammation?
Results in the production of inflammatory mediators.
183
What do inflammasome receptors detect as part of the acute inflammatory response?
They recognise multi protein cytoplasmic complexes and products of dead cells.
184
What is the outcome of using inflammasome receptors in the acute inflammatory response?
They activate caspace-1 which activates mediators of leukocyte recruitment. The recruited leukocytes then phagocytose and destroy the injurious agent or dead cells.
185
Outline the life cycle of a B lymphocyte duding interphase.
```
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.
```
186
What do B lymphocytes derive from and where are they produced?
Stem cells
| Bone marrow
187
How do B lymphocytes move around the body?
Via the blood
188
Where are B cells stored ?
The lymphatic system
189
What part of the B cells allows activation by antigens?
B cells immunoglobulin on their membrane. This can be activated to induce differentiation.
190
How long do plasma cells generally survive for?
1-2 weeks
191
How long do memory cells generally survive for?
Decades
192
What do B lymphocytes divine into?
Plasma cells and memory cells
193
What are the 3 different types of lymphocytes ?
B cells, T cells, Natural Killer cells (NK cells).
194
Are B and T lymphocytes part of the specific or non-specific immunity?
Specific
195
Where do T and B cells migrate to from the bone marrow?
Lymphatic system
196
What are T and B cells activated by ?
Antigens
197
Are Natural killer cells part of specific or non-specific immunity?
Non-specific
198
Where are clusters of differentiation found?
Antigens on the surface of lymphocytes
199
How are CD antigens used to identify cell types which are present in a sample - outline the process.
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.
200
What cell type are CD4 antigens used to identify?
Helper T cells
201
What cell type are CD8 antigens used to identify?
Cytotoxic T cells
202
What cell types are CD21 antigens used to identify?
B cells
203
Outline the life cycle of a T lymphocyte.
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.
204
Which specific antigens can T lymphocytes recognise?
Antigens displayed alongside MHC molecules.
205
Which specific antigens can B lymphocytes recognise ?
All free antigens
206
What type of CD antigen markers do helper T cells have and what type of MHC antigens do they recognise?
CD4
| MHC classII
207
What type of CD antigen markers do cytotoxic T cells have and what type of MHC antigens do they recognise?
```
CD8
MHC class I
```
208
What type of CD antigen markers do regulatory T cells have ?
Some have CD4 and are therefore MHC class II restricted. Others have CD8 and are therefore class I restricted.
209
What are major histone complexes?
Tightly linked clusters of genes present in every mammalian species.
210
Which chromosome are major histone complexes present on in humans?
6
211
What are polymorphic genes?
There are multiple alleles for each genes
212
What are halotype inherited genes?
A group of genes within an organism that have been inherited from only one parent.
213
Where are polymorphic genes often present?
Oh major histone complexes.
214
What does MHC stand for?
Major histone complexes.
215
What type of antigens are presented to helper T cells?
Exogenous
216
How do antigen presenting cells work?
They present a fragment of the antigen associated with an MHC molecule on their plasma membrane surface.
217
What are endogenous antigens?
They original inside the body and create complexed with MHC class I proteins.
218
What cell type are endogenous antigens recognised by ?
Cytotoxic T cells
219
What are exogenous antigens?
They originate outside the body and create complexes with MHC class II proteins.
220
What cell type are exogenous antigens recognised by?
Helper T cells
221
Which MHC class do exogenous antigens create complexes with?
MHC class II
222
Which MHC class do endogenous antigens create complexes with?
MHC class I
223
What are the 3 types of antigen presenting cells.
Macrophages
Dendritic cells
B cells
224
How do macrophages present antigens ?
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
How do dendritic cells present antigens?
```
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
How do B cells present antigens?
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
What type of MHC molecules are always carried on antigen presenting cells ?
Class II
228
What is the overall, general purpose of cell-mediated immunity?
To kill foreign or abnormal cells.
229
What are the 3 ways that cytotoxic T cells kill ?
| Give a brief outline of each.
Cytolysis - release perforin
DNA fragmentation - Release lymphotoxin which fragments nuclear DNA.
Phagocytosis - Release gamma interferon which enhances phagocytic activity of macrophages.
230
When do T cells move from their immature to mature form?
When they are activated by antigens.
231
Outline the process of T cell activation for CD4 T cells.
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
What are the differences between CD4 and CD8 T cell activation ?
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
What is proliferation?
To multiply rapidly
234
What would occur if costimulation of T cells didn't occur?
T cells would remain in a prolonged state of inactivity known as anergy.
235
What is anergy?
Absence of the normal immune response to a particular antigen - T cells are never activated.
236
What is the purpose of costimulator molecules?
They allow T cells to adhere to the antigen presenting cell for a longer amount of time.
237
What type of molecules are costimulator molecules?
Cytokines or a pair of plasma membrane molecules.
238
What is the recruitment of leukocytes during acute inflammation controlled by?
Adhesion molecules and Chemokines
239
What is the general purpose of Chemokines duding acute inflammation?
They arrant cytokines which aids migration of leukocytes to the site if inflammation.
240
Name the steps of migration of leukocytes during acute inflammation.
```
Margination
Rolling
Adhesion
Diapedesis
Chemotaxis
```
241
Outline the process of margination of Leukocytes during acute inflammation.
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
Outline the process of rolling in migration of Leukocytes during acute inflammation.
Leukocytes bind to an epithelial cell. They then detached and bind to an epithelial cell further down the blood vessel.
243
What is the rolling of Leukocytes in acute inflammation controlled by ?
P, E and L selectin molecules.
244
Describe the binding of selectin molecules to Leukocytes.
Low affinity
245
Outline the adhesion process of Leukocyte migration during acute inflammation.
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
What are the 2 types of intern ligand?
Vascular cell adhesion molecules (VCAM-1)
| Intracellular adhesion molecules (ICAM-1)
247
Outline the Diapedesis process of migration of Leukocytes during acute inflammation.
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
What is the Diapedesis process during migration of Leukocytes controlled by?
PECAM molecules - Plateles cell adhesion molecules
249
Outline the mechanism for chemotaxis of leukocytes during acute inflammation.
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
What is meant by the term localisation?
The movement of a specific substance to a specific region.
251
What is extending filopodia?
Migrating cells use cytoplasmic projections called micro spikes to form adhesions with the cell surface membrane and therefore move.
252
What type of receptors are used to detect foreign bodies during acute inflammation?
Phagocytic receptors (Mannose receptors, Scavenger receptors, Opsonin receptors).
253
What are the 3 types of phagocytic receptors used to detect foreign bodies in acute inflammation?
Mannose receptors, Scavenger receptors and Opsonin receptors.
254
What are the purpose of mannose receptors during acute inflammation?
They bind to terminal mannose and residues of glycoproteins and glycoplipids which are found in microbial walls.
255
What is the purpose of scavenger receptors in acute inflammation
They bind to modified low density lipid molcules found within lipids.
256
What is the purpose of opsonin receptors in acute inflammation?
They recognise opsonins which are antibodies which bind to forming microorganisms and make them more susceptible to phagocytosis.
257
What are opsonins?
Antibodies which bind to microorganisms and make them more susceptible to phagocytosis.
258
What 3 main things can happen when Leukocytes are activated during acute inflammation?
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
What are the differences between phagocytosis and pinocytosis ?
```
Phagocytosis = engulfment of debris, bacteria and other objects.
Pinocytosis = Engulfment of extracellular fluid.
```
260
Outline the process of phagocytosis during acute inflammation.
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
Outline how reactive oxygen species are used to kill microbes in the phagolysosome during acute inflammation.
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
How does the polyclonal nature of antibodies affect the amount of antigen dilutions required in the precipitation ring reaction?
No effect
263
What type of immunity are the compliment systems part of ?
Innate
264
Where are most compliment proteins produced ?
The liver
265
How does the classical compliment pathway eventually kill pathogens?
It forms a C5b6789 membrane attack complex via a cascade system.
266
How does the alternative compliment pathway eventually kill pathogens?
It requires spontaneous hydrolysis of C3 compliment protein. This then triggers a cascade system to produce C5b6789 membrane attack complex.
267
What triggers the alternative compliment system?
```
Bacteria endotoxins (lipopolysaccharides in the outer membrane of bacteria).
Yeast cell walls.
```
268
What does the lectin mannose compliment pathway require to continue?
Requires mannose binding lectin protein
269
Where is mannose binding lectin protein produced?
The liver
270
How is the lectin mannose compliment pathway triggered?
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
What are the immune effects of compliment products?
Opsonisation
Cell lysis
Chemotaxis
Mass cell production
272
How do compliment systems cause opsonisation?
C3b activates neutrophils and macrophages to engulf the invading pathogen by phagocytosis.
273
How do compliment systems cause cell lysis?
They produce membrane attack complexes which rupture (bacterial) cell walls.
274
How do compliment systems allow chemotaxis and how is this helpful?
C5a attracts neutrophils and macrophages to the invading antigen for phagocytosis.
275
How do compliment systems enable mast cell production and how is this helpful?
Some compliment protists activate make cells and basophils which mediate inflammation.
276
What causes immunological memory?
Long-lived antibodies
Memory T and B cells
Affinity maturation
277
How do Memory T and B cells cause immunological memory?
They last years/decades. Upon re-exposure to the same antigen a greater, faster, more long-lasting secondary response occurs.
278
What is affinity maturation in terms of immunological memory?
Produces antibodies which have a greater affinity to the antigen and therefore aids the immunological response.
279
Give an example of a process which allow affinity maturation of antibodies
The antibodies may undergo a 'class switch' which allows the antibodies to have a greater affinity to the antigen.
280
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?
Host cells block themselves using secretory IgA antibodies. However bacteria contain proteases that split IgA dimers.
281
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?
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
How do bacterial cells evade the process of compliment-mediated lysis?
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
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?
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
How does the humeral immune response prevent viruses harming the host?
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
How do complement systems prevent damage to the host by viruses?
Complement systems assist opsonisation and produce membrane-attack complexes which help to kill host cells infected with the virus.
286
Can membrane attack complexes directly kill viruses?
No they must produce a membrane attack complex which helps kill the virus.
287
How does the immune system use gamma interferons to prevent damage by viruses? What type of immune response is this?
Cell-mediated response.
| Gamma interferons act as a direct antiviral agent to stop virally infecting cells replicating.
288
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?
They cells kill cells which have been infected with the virus.
Cell mediated response
289
How do some viruses prevent the complement cascades?
They bind to complement components and therefore prevent the compliment cascade.
290
How do viruses cause antigenic drift?
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
How is antigenic drift beneficial to viruses?
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
How do viruses cause antigenic shift?
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
What methods do parasites use to evade the immune system?
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
What is anaphylaxis?
A serious allergic reaction that is rapidly onset and may cause death.
295
What are dimers?
2 identical molecules linked together.
296
What are the main functions of the blood?
Transports (dissolved gases hormones, nutrients, heat, waste).
Regulation (pH, temperature, absorption, blood flow, osmosis).
Protections (forms clots, transports WBC's).
297
Describe the viscosity of the blood in comparison with water.
More viscous
298
What should the temperature of the blood be?
37 digress celcius
299
Describe the pH generally of blood.
Slightly alkaline.
300
Describe the colour of the blood when saturated and un-saturated with oxygen.
```
Saturated = Bright red
Un-saturated = Dark red
```
301
What % of body mass is the blood?
8
302
What hormones regulate blood volume and osmotic pressure?
Aldosterone
ADH
Anti-natiuretic peptide
303
What plasma proteins are in the blood? (4)
Albumins
Globulins
Fibrinogens
Regulatory proteins
304
What do albumin plasma proteins do?
Control blood osmolarity
305
What do globulin plasma proteins do?
Transport ions, hormones, lipids and have immune functions.
306
What do fibrinogen blood proteins do?
Essential component of the clotting system.
307
What are the purpose of electrolytes in the blood?
Aid vital cellular activities and contribute to osmotic pressure of the body
308
What are organic nutrients in the blood used for?
The are used for ATP production and growth and maintenance of cells.
309
What are the purpose of anticoagulants in a blood sample?
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
What is used to keep a blood sample in liquid form?
Anticoagulants
311
What is haematology?
A form of healthcare concerned with diagnosing and monitoring diseases of the blood and blood forming organs.
312
What are MHC levels of the blood?
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
What is erythrocyte sedimentation rate a measure of ?
An indirect measure of inflammation
314
How may erythrocyte sedimentation rate alter during inflammation?
The number of red blood cells will fall more rapidly than usual.
315
What is coagulation screening used to identify?
Bleeding issues with the blood.
316
What are haematinic assays used for?
They measure factors involved with red blood cell production to identify issues such as anaemia.
317
What are the medical uses of immunophenotyping?
Used to identify haematological malignancies.
| Can identify the size and complexity of different cells
318
What are the uses of electrophoresis in terms of the blood?
They are used to identify the different types of haemoglobin in a blood cells. Can identify diseases cause by haemoglobin.
319
What technique can be used to identify sickle cell anaemia?
Electrophoreis.
320
Which blood components maintain osmotic pressure?
Albumins
321
What vacutainer should be used to collect a sample for syphillis analysis?
Gold
322
What type of feedback controls red blood cell and platelet count in the blood?
Negative.
323
What causes white blood cell numbers in the blood o fluctuate?
Infection
324
What is the technical name for the formation of blood cells?
Haemopoiesis
325
What is Haemopoiesis?
The formation of blood cells
326
Where are red blood cells formed ?
Red bone marrow
327
What causes red bone marrow to become yellow?
Fatty deposits accumulate over time.
328
What can cause yellow bone marrow to become red again?
Trauma
329
Where are plutipotent stem cells found?
Red bone marrow
330
How does the bone marrow of patients with leukaemia differ from healthy bone marrow?
Leukaemia patients will have large leukaeamic blasts forming.
331
What types of diseases can red bone marrow examination identify?
Anaemias, proliferate malignancies, leukaemia, cell morphology changes.
332
What subtypes of stem cells do pluripotent stem cell produce?
Myeloid stem cells and lymphoid stem cells
333
Where do myeloid stem cells develop?
Red bone marrow
334
What cell types do myeloid stem cells give rise to?
Platelets, red blood cells, monocytes neutrophils, eosinophils and basophils.
335
What cell types of lymphoid stem cells give rise to?
Lymphocytes.
336
Where do lymphoid stem cels develop and where do they end up?
Develop = red bone marrow
| End up = lymphatic system
337
What are pluripotent stem cells?
Can differentiate into any cell type.
338
What are the purpose of erythropoietin?
They make myeloid stem cells differentiate into red blood cells.
339
What makes myeloid cells differentiate into red blood cells?
Erythropoietin
340
Where is erythropoietin produced?
Kidneys
341
What is the purpose of thromopoeitins?
They cause myeloid cells to differentiate into platelets.
342
What causes myeloid cells to differentiate into platelets?
Thrombopoietins
343
What is the purpose of the lymphatic fluid?
Carries waste products around the body.
| Carries cells that are part of the immune system.
344
What takes lymph fluid to the lymph nodes?
Lymph vessels
345
What are progenitor cells and what cell type do they derived from?
Derive from myeloid stem cells.
| Cannot reproduce but form CFU and CFU-E cell types.
346
What are precursor cells and what cell type do they derive from?
Precursor cells develop into formed elements of the blood over many divisions.
347
What can CFU cell types be recognised by?
Can't be recognised by microscopy.
| Can be recognised in bone marrow biopsies.
348
Why can CFU cells be recognised in bone marrow biopsies?
They are large and have a high nuclear/cytoplasm ration.
349
How might kidney failure affect blood cell formation and what are the physiological effects of this?
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
What is one of the main symptoms of anaemia?
Fatigue
351
What will be the consequence of lowered Thrombopoietin production?
Fewer myeloid stem cells will differentiate into platelets which may cause issues with blood clotting and lead to excessive, extended periods of bleeding.
352
What is the usual life span of a platelet?
5-9 days
353
What are the 3 main stages of Haemostasis ?
Vascular spasm
Platelet plug formation
Blood Clotting
354
What are the main purposes of mast cells?
Dilate blood vessels.
Releases histamines and Herapins to induce inflammation.
Recruits macrophages and neutrophils.
Often responsible for allergic reactions.
355
Where are mast cells found?
Connective tissues
| Mucous membranes
356
What are the main purposes of macrophages?
Phagocytosis of foreign pathogens.
| Stimulates the response of other immune cells
357
What are the main purposes of monocytes?
Differentiate into macrophages and dendritic cells in response to inflammation.
358
Where are monocytes found?
They are stored in the spleen but move through the blood vessels to the required tissues.
359
What are the main purposes of neutrophils.
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
What are the main purposes of basophils?
Responsible for defence against parasites. Release histamines that cause inflammation and are often responsible for allergic reactions.
361
What are the main purposes of Eosinophils?
Release toxins that kill bacteria and parasites but also cause tissue damage.
362
What is the purpose of red blood cells having no nucleus?
Saves space for more haemoglobin to be present and therefore the ability to carry more oxygen or carbon dioxide.
363
What is the purpose of the red blood cells having no mitochondria?
They don't use oxygen and only do anaerobic respiration so the oxygen they carry will be transported to other body parts.
364
What is the purpose of Nitric Oxide in the blood?
Vasodilation.
| Thrombotic control - control of blood clotting. Prevents the blood agglutinating when it shouldn't.
365
What is thrombotic control?
Control of blood clotting.
366
What is the purpose of carbonic anhydrase in red blood cells?
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
What effect does testosterone have on redd blood cell production and how?
Causes Erythropoietin to be produced so more myeloid stem cells differentiate into red blood cells.
368
What is Haematocrit?
The ratio of the total volume of red blood cells to the total volume of the blood.
369
What causes Polycythaemia?
When too many red blood cells are present in the blood and causes blood viscosity to become too high.
370
What happens when a person has Polycythaemia? (symptoms)
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
What is meant by the term 'hypoxia' ?
Deprived of oxygen
372
What causes neutrophil counts to increase and decrease?
```
+ = Bacterial infection, stress, burn, inflammation.
- = Radiatioon exposure
```
373
What causes lymphocyte counts to increase or decrease?
```
+ = Viral infection, some Leukaemias.
- = Prolonged illness, immunosupression
```
374
What causes monocyte counts to increase or decrease?
```
+ = Viral or fungi infection, some chronic illnesses.
- = Bone marrow suppression.
```
375
What causes Eosinophil count to increase or decrease?
```
+ = Allergic reactions, parasitic infections.
- = Toxic drugs, stress
```
376
What causes Basophil count to increase or decrease?
```
+ = Allergic reactions, leukaemia, cancer
- = Pregnancy, ovulation, stress
```
377
How high a suspected cause of Polycythaemia be investigated?
Carrying out a red blood cell count. Excessive red blood cells could indicate polycythaemia.
378
How may an elevated basophil count become apparent?
Excessive and un-necessary inflammation.
379
On a blood smear lots of cells with lightly stained granules and multi-lobed nuclei are found. What are these likely to be ?
Neutrophils or Eosinophils.
380
What is blood doping?
A way of improving athletic performance by artificially boosting the blood's ability to bring more oxygen to the muscles.
381
What do type 1 interferons stimulate the synthesis of?
Anti-viral proteins
382
What part of immunity do type 1 interferons belong to?
Natural
383
What cell types produce type 1 interferons?
Macrophages
384
Is an adaptive immune response capable of memory?
Yes
385
Neutrophils secrete a greater variety of substances. than macrophages. True or False?
False
386
Do antigenic molecules contain amino acids? and if so, what type?
Yes - likely to be aromatic
387
Are antigenic molecules likely to be soluble or insoluble?
Insoluble
388
Are antigenic molecules likely to contain simple or complex sugars?
Complex
389
What does primary immunodeficiency arise from?
Infections
390
Can primary immunodeficiency arise from complement defects?
No
391
What is the site of maturation for the lymphocyte subset?
Thymus
392
What filters out microorganisms which have been washed up by the lymphatics into the interstitial fluids?
Lymph nodes
393
What are the purpose of the lymph nodes?
They filter out microorganisms which have been washed up by the lymphatics into the interstitial fluids.
394
After how many hours does acute inflammation peak?
24
395
What is the purpose of the spleen in terms of immunology?
Is the main lymphoid tissue to protect against blood-born antigens.
396
What is the main lymphoid tissue to protect against blood-born antigens?
The spleen
397
How do tonsils aid immunology?
Protect against oral and nasal pathogens.
398
What is the purpose of the Mucosa-associated lymphoid tissue? (MALT)
Defends the lining of externally opening organs.
399
How does the herpes simplex virus prevent an immune response generally?
Inhibits antigen processing
400
How does the vaccinia virus prevent an immune response?
Binds to complement components
401
How does Hepatitis virus C prevent an immune response?
Blocks interferons
402
How does HIV prevent an immune response?
Reduces MHC class II
403
How does adenovirus prevent an immune response?
Reduces MHC Class I
404
Does MAC or perforin cause cytolysis?
Both
405
How many epitopes do monoclonal antibodies bind to?
1
406
What cell type are monoclonal antibodies produced by?
A single B cell clone
407
What is the overall purpose of the acute phase response?
A means of reducing bacterial toxicity and limiting tissue damage.
408
What is the acute phase response mediated by?
Macrophage cytokines.
409
Describe the relative sizes of neutrophils and macrophages.
Neutrophils are smaller.
410
Describe the relative lengths which neutrophils and macrophages last in circulation.
Macrophages last longer.
411
What chemical is produced when cytotoxic T cells are activated?
Perforin
412
What is the purpose of interleukin 2 ?
An autocrat stimulator of helper T cells.
413
What type of cells does Costimulation require?
Antigen-presenting cells
414
Which MHC class associated antigens do macrophages present?
MHC class II
415
What type of cytotoxic T cells does interleukin 2 costimulate?
Antigen-bound cytotoxic T cells
416
What type of interferons do activated cytotoxic T cells produce?
Gamma interferons
417
When type 1 interferons are stimulated, what type of proteins do they produce?
Anti-viral
418
What mediates the acute inflammatory response?
Complement
419
Activation of complement results in perforin production - true or false?
False
420
What MHC class do endogenous antigens complement with ?
MHC class I
421
What cell type are endogenous antigens recognised by?
Cytotoxic T cells
422
How do natural killer cells kill pathogens (generally)?
Release perforin
423
What cells release histamine?
Mast cells
424
In the tethering process of platelet formation, outline the process, what extracellular matrix protein is required and the receptor needed.
Platelet binds to exposed extracellular matrix and therefore stops moving.
This requires vWF which is stuck on collagen.
Receptor: GpIb/v/IX
425
In the activation process of platelet formation, outline the process, what extracellular matrix protein is needed, what receptor is needed.
Platelets release granule content, spread and adhesion receptors are activated.
ECM collagen needs.
Receptor: GPVI
426
In the adhesion process of platelet formation, outline the process, what extracellular matrix protein is needed and what receptor is needed.
Single layer of platelet binds to the extracellular matrix.
Collagen
Receptor: a2B1
427
In the secretion process of platelet formation, what happens?
Platelets release the platelet activating chemicals ADP and TxA2.
428
In the aggregation process of platelet formation, what happens, what extracellular matrix proteins is required and what receptor is required?
Multiple layers of platelets bind to each other.
Fibrinogen required
Receptor: aIIbB3
429
What are the 3 main types of haematological malignancies?
Common Leukaemias.
Myeloproliferate Neoplasms.
Multiple Myeloma.
430
What are Leukaemias?
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
What is meant by the term 'malignant' in terms of cells?
Cells that divide without control.
432
What are Lymphomas?
Cancers with a lymphoid origin.
433
What are some symptoms of Leukaemia?
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
Why does Leukaemia cause swelling of the lymph nodes, spleen and liver.
These areas will overcompensate and try to make excess red blood cells when tumours are present.
435
What characterises acute Leukaemia?
Immature immune blast cells make up at least 20% of the nucleated cells in the bone marrow.
436
Other than high blast count in the bone marrow, what else can indicate acute Leukaemia?
Evidence of arrest of immune cell maturation.
437
Is chronic or acute Leukaemia more aggressive?
Acute
438
What characterises chronic Leukaemia?
Have less than 20% of immature blast cells making up their nucleated cells in the bone marrow.
439
Why do malignant cells accumulate in chronic inflammation?
Cells don't do apoptosis
440
Does maturation arrest of immune cells occur in acute or chronic Leukaemia?
Acute
441
What are the 2 main derivatives of Leukaemia?
Myeloid
| Lymphoid
442
What is meant by a Leukaemia being myeloid?
Arising from neutrophil, monocyte, basophil or eosinophil pre-crusor cells.
443
What is meant by a Leukaemia being lymphoid?
Arising from B-lineage or T-lineage lymphocytes, Natural killer cells or their pre-cursors.
444
What are the 4 overall types of Leukaemia?
Acute lymphoblastic Leukaemia.
Chromic lymphocytic Leukaemia.
Chronic Myelogenous Leukaemia.
Acute Myelogenous Leukaemia.
445
In what people is Acute Lymphoblastic Leukaemia most common ?
Children
446
What is the onset relative time of acute lymphoblastic leukaemia?
Short onset
447
In what people is Chromic lymphocytic Leukaemia most common?
Adults 55+
448
What people does Acute myelogenous Leukaemia affect most?
All ages
449
Describe the relative onset time of chronic myelogenous Leukaemia.
Long onset time
450
What type of people does Chronic myelogeonous Leukaemia mostly occur in?
Adults
451
Why do cancer cells produce excessive white blood cells?
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
What are the risk factors and possible causes of Leukaemia?
Radiation exposure, smoking, genetic disorders, benzene.
453
Why are people who have previously had cancer more likely to get a different type of cancer ?
Cancer treatments can be a risk to causing other tumours of different types.
454
What are the causes of Acute lymphocytic leukaemia?
Chromosomal mutations resulting in abnormal transcription factors that affect the development of B and T cells.
455
What are the cells involved in acute lymphocytic Leukaemia?
Immature T and B cells.
456
What are the causes of Chromic Lymphocytic Leukaemia?
Chromosomal deletion or point mutations of the B cells.
457
What cell types does Chronic Lymphocytic Leukaemia affect?
Peripheral T and B cells in the lymph nodes
458
Explain the difference of how common Chronic Lymphocytic Leukaemia is in women and men.
Twice as common in men.
459
What are the causes of Acute Myelogenous Leukaemia?
Onocgenic mutations impede differentiation meaning that immature myeloid blasts accumulate in the bone marrow.
460
What are the common symptoms of Acute Myelogenous Leukaemia?
Anaemia, Spontaneous bleeding.
461
What are the causes of Chronic Myeloid Leukaemia?
Thyrosine kinase pathway related chromosomal translocation - Philadelphia chromosome.
462
What cells are affected in chronic myeloid leukaemia?
Pluriptotent hematopoetic stem cells.
463
What are the common symptoms of chronic myeloid leukaemia?
Slow onset, mild anaemic symptoms.
464
What are the common symptoms of acute lymphocytic Leukaemia?
Fast onset, depressed bone marrow function, bone pain
465
What are the common symptoms of chronic lymphocytic leukaemia?
Asymptomatic or non-specific symptoms
466
What is the Philadelphia chromosome and how does it cause Leukaemia?
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
On what chromosome is the ABL1 gene?
9
468
on what chromosome is the BCR gene?
22
469
What are bone marrow transplants used for?
To replace cancerous red bone marrow with healthy red bone marrow.
470
What medication must a patient be taking during a bone marrow transplant?
The patient must stay on immunosuppressants.
471
What methods are used to destroy unhealthy red bone marrow in a bone marrow transplant?
Chemotherapy or whole body radiation.
472
What is Leukaemia?
The presence of malignant Leukocytes within the blood or bone marrow that suppress the production of other cells.
473
What are Myeloproliferate Neoplasms in general?
A group of rare disorders of the bone marrow that cause in increase in the number of blood cells produced
474
How many different types of blood cell are produced in excess when a person has myeloproliferate neoplasms?
1 or more
475
What are myfibroblasts?
Cells that synthesise collagen for the extra-cellular matrix.
476
What (in general) is Thrombocythemia?
A blood disorder that causes an extremely high number of platelets to be produced.
477
Why do people experience abrnomal bleeding if they have thrombocythemia?
Platelets produced are not maturing properly so don't function effectively.
478
What causes patients with thrombocythmia to experience dizziness, headaches, fainting etc?
Blood clots forming in several organs of the body.
479
What causes patients with thrombocythemia to experience ministrokes?
Blood clots in arteries that supply the brain.
480
What is the main cause of Polycythemia Vera?
JAK2 mutation
481
What is Polycythemia Vera (overview)?
Slow-growing blood cancer where the bone marrow produces too many red blood cells.
482
Why do people with Polycythemia Vera have low levels of EPO?
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
What mechanism does the JAK2 mutation in patients with Polycythemia Vera affect?
It affects the Thyrosie Kinase receptor signalling pathway and causes cells to proliferate un-necessarily.
484
How would the blood film of an individual with Thrombocythemia be different than a normal blood film?
Aggregations would occur - clotting would show.
| More platelets would be visible.
485
What is Myelofibrosis in general?
A rare condition affecting the bone marrow. Scar tissue builds up inside the bone marrow meaning that blood cells aren't made properly.
486
Why do the spleen and liver become enlarged in patients with Myelofibrosis?
The liver and spleen try to compensate for the lack of blood cells being produced by the bone marrow.
487
What is primary Myelofibrosis?
People who haven no history of problems with their bone marrow getting myelofibrosis.
488
What is secondary myelofibrosis?
Where primary myelofibrosis developes in people who already have issues with their bone marrow.
489
What type of Leukaemia is sometimes acquired by individuals with myelofibrosis?
Acue Myeloid Leukaemia
490
What causes thick, coarse fibres to to form in the bone marrow during Myelofibrosis?
Increased expression of inflammatory cytokines from mutated megakaryocytes and other platelet forming cells.
491
What replaces the bone marrow over time when a patent has Myelofibrosis?
Thick coarse fibres
492
What happens to the production of blood cells over time when a patient has Myeloifibrosis and why?
Coarse fibres replace the bone marrow meaning fewer number of blood cells are produced. This results in anaemia.
493
what are some of the symptoms of Myelofibrosis?
Fatigue, bone pain, night swears, fever.
494
What are pulmonary embolisms?
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
What is cytopenia?
A reduction in the number of mature blood cells.
496
What cells does multiple myeloma affect?
Plasma cells of the bone marrow.
497
What environmental risk factors are associated with multiple myeloma?
Herbicides, insecticides, benzene, hair dyes and radiation
498
What is the cause of multiple myeloma?
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
What are the symptoms of multiple myeloma?
Weakened bones, easily broken and fractured bones, anaemia.
500
What is osteoporosis?
Bone thinning and weakening
501
What causes thickened blood in people with multiple myeloma?
Vast production of 'M protein'.
502
What methods are used to treat multiple myeloma?
Chemotherapy drugs, radiation therapy, stem cell transplants and taking drugs that modulate the immune system.
503
What is cell morphology ?
The specific phenotype of a cell ; shape, structure, form and size.
504
What are haematological malignancies?
Cancers that begin in the cells which are then subdivided according to the type of blood being affected.
505
What are MHC levels?
The average haemoglobin in each red blood cell.
506
What are MHCH levels?
The average weight of haemoglobin present based on the volume of red blood cells.
507
What is cytometry?
Determining the size, shape and nucleic acid content of cells using a flow cut-meter.
508
What is a blood film used to identify?
Altered numbers and staining to diagnose diseases such as anaemia and leukaemia.
Morphology changes that indicate genetic disorders.
509
What Can a full blood count identify?
No of cells of each type.
MHC levels.
MHCH levels.
Therefore altered functioning or presence of red blood cells and haemoglobin.
510
What do erythrocyte sedimentation rate experiments identify and what does this help identify?
Measures the mm of clear blood plasma in the top of a column after one hour. Indirectly measures inflammation.
511
What does a coagulation screen identify?
Identifies if bleeds are due to deficiencies in the common, intrinsic or extrinsic coagulation pathways.
512
What are haematological assays and what can they identify?
Measures factors that are involved with control of red blood cell production.
Used to investigate treatments for anaemia.
513
What is immunophenotyping?
Using flow cytometry to analyse proteins on the surface of white blood cells.
514
What is immunophenotyping used to identify?
Haematological malignancies.
515
What can be identifies using haemoglobin variation detection by gel electrophoresis?
Analyses malignant cell types and identifies sickle traits.
516
How does nitric oxide affect platelet adhesion?
Reduces it
517
Which type of leukaemia is the Philadelphia chromosome associated with?
Chronic myeloid leukaemia
518
Which type of leukaemia is essential thrombocythemia associated with?
Chronic myeloid neoplasms
519
What is the main feature of essential thrombocythemia?
Excess platelets
