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Pathology and Immunity > Tutorial Answers > Flashcards

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1
Q

what is provisional diagnosis based on

A

symptoms
signs
history

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2
Q

how does a surgical seive aid in diagnosis

A

helps in the narrowing down of disease responsible.
oral clues may also provide evidence of other underlying diseases whcih in turn may lead to manifestations in the oral cavity.

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3
Q

what can be done to aid in patient diagnosis following a provisional diagnosis

A

refer to a specialist, order a biospy or other clinical tests

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4
Q

what biological process causes the redness of gingiva

A

inflammation

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5
Q

what are the basic stages of inflammation

A
  • initiation of reaction (response to harmful agents)
  • progression (containment of harmful agents)
  • amplification (modulation of immune response)
  • resolution (favourable outcome leading to healing)
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6
Q

how does the oral epithelium and saliva protect against infection by pathogenic bacteria that may be present in the dental plaque

A

gum tissue acts principally as a physical barrier, a number of antimicrobial products are produced by cells and also in the gingiva to protect the tissue

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7
Q

what are some key molecules found in the saliva that aid in the protection of the mouth

A
  • lactoferrin
  • lysozyme
  • peroxidase
  • antimicrobial peptides
  • immunoglobins
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8
Q

what is the function of lactoferrin

A

glycoprotein that transports ions but has antimicrobial activity
present in the saliva and produced by neutrophils

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9
Q

what is the function of lysosyme

A

present in the saliva and produced by macrophages and neutrophils
targets cell walls of bacteria

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10
Q

what is the function of cystatins

A

anti protease activity and supports remineralisation of the teeth

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11
Q

what are the major families of antimicrobial peptides found in the saliva

A

b defensins
human neutrophil peptides
cathelicidins

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12
Q

how does the body identify potentially harmful organisms in dental plaque, what types of receptors are involved, and what do they recognise?

A

pattern recognition receptors like toll like receptors and pathogen associated molecular patterns, activation leads to change in cell phenotype and the production of inflammatory mediators

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13
Q

wha tis the basic function of neutrophils

A

produce NETs

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14
Q

what is the main function of macrophages

A

phagocytosis and antigen presentation

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15
Q

what is the main function of dendritic cells

A

phagocytose and present antigen

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16
Q

what is the main function of mast cells

A

degranulate to release histamine and antimicrobial agents

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17
Q

what is the main function of b cells

A

produce antibodies

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18
Q

what is the main function of t cells

A

to drive cell mediated responses

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19
Q

can you describe how the immune cell populations within the gingival tissues differ during the early inflammatory response compared to a later chronic inflammatory response

A

early inflammation is mainly macrophages and neutrophils
later there are more b cells and t cells

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20
Q

how do both myeloid and lymphoid cells originate

A

both lineages from common stem cell precursors form myleoid and lymphoid stem cell progenitors in the bone marrow

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21
Q

what roles do the thymus, lymph nodes and spleen play in immune cell function

A

these are organs of the immune system
the thymus is where t cells mature
the lymph nodes and spleen are reservoirs of immune cells

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22
Q

what are Il6 and Il1beta

A

cytokines, signalling molecuels that coordinate immune response

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23
Q

what are the families of cytokines

A

interleukins
tnf family
interferons

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24
Q

why can interleukin levels in a periodontitis patient be raised

A

there is elevated localised production of interleukins at the inflammatory site that enter their way into the circulation. give information to dictate immune response, and cytokine production can be related to the type of threat and tell the body how to respond

25
explain the processes involved in the activation of complement
there are three pathways determined by the initiating factor - classical complement pathway binds via the antibody IgG or IgM coating the bacterial surface - alternative complement pathway is when C3b binds directly to the cell wall of a microbial cell - lectin pathway is when complement proteins bind to the mannose binding lectin on the cell surface
26
what is mannose
a carbohydrate on the surface of microbial cells
27
what is the process of complement activation
involves proteins enzymes and subsequent fragments following enzymatic degradation eg C3 splits into C3a and C3b and C5 splits into C5a and C5b C3/5a are anaphylatoxins with multiple functions within the immune system such as increasing vascular permeability and increasing cellular migration
28
what is the result of complement activation
formation of the membrane attack complex form pores on the surface of the bacteria which drives lysis of the cell anaphylatoxin production
29
explain the process by which circulating neutrophils are recruited to the site of infection
cell adhesion molecules control interactions between immune cells like neutrophils and endothelial cells which move against the chemokine gradient and undergo diapedesis through interactions between receptors on immune cells and receptors on endothelial cells
30
what are the three main families of cell adhesion molecules
selectins integrins immunoglobin superfamily
31
describe the production of chemokine gradients during inflammation
chemokines are released by cells at the site of infection due to endocrine nature they will enter the circulation and create a gradient so there is high interleukin concentration in the tissue and low in the blood and the cells will move toward the higher concentration
32
what are the other effector functions of neutrophils aside from engulfing and destroying invading pathogens by phagocytosis
- degranulation due to granules in cell vesicles containing numerous antimicrobial peptides and enzymes that are released upon activation of receptors - production of neutrophil nets - the activation of neutrophils releases proteins and some genetic material to form extracellular fibril matrix - these trap pathogens whilst granule release leads to antimicrobial activity
33
what is an antigen
a substance which triggers a specific immune response
34
what is an antigen presenting cell
cells which present antigens to the adaptive immune response
35
how do antigen presenting cells process antigens
they are constantly processing them in tissues in both health and diseased states they are loaded onto either MHC1 if they are endogenous or II if they are exogenous
36
which t cells get antigens from MHC1
CD8
37
which t cells get antigens from MHC2
CD4
38
how do dendritic cells activate naive t cells to initiate a primary adaptive immune response
dendritic cells take up and process the antigen at the mucosal barrier surface once they have taken up the antigen they migrate to lymph nodes and mature en route dendritic cells have co stimulatory activity and can prime naive t cells in specific regions of the lymph node
39
what is t cell priming
this is when a naive t cell, after undergoing education in the thymus, residingin the lymph nodes, interacts with dendritic cells. three signals are critical for activation and differentiation into subsets
40
what is signal one of t cell priming
activation of the t cell via MHC-TCR interactions
41
what is signal two of t cell priming
survival and clonal expansion of t cells driven by co stimulatory molecules
42
what is signal three of t cell priming
differentiation into subsets for CD4 cells. for CD8 cells, the third signal is an effector function of destruction of infected cells, and all nucleated cell types have an ability to present an antigen via the MHC1
43
which t cell subsets can initiate the adaptive immune response
CD4
44
explain how a t cell with a receptor specific for the clostridium tetani antigen is developed from a pre thymic t cell in the thymus
t cells will interact with thymic cortical epithelial cells in the thymus needs to be of a level of moderate binding so the t cell receptor recognises the MHC molecule in positive selection, if there is no recognition at all the cells are destroyed via apoptosis in negative selection, if the TCR binds too strongly to the self peptide then the t cell is also removed via apoptosis t cell receptors are generated through the process of somatic recombination
45
what are the basic principles of vaccination
used to elicit a primary response to a pathogen to form immunological memory in the form of memory b cells which will protect the host upon re encounter with the antigen it involves class switching of IgM to IgG antibody in the memory b cells to produce a more effective, stronger response upon re exposure
46
explain how vaccination activates a specific b cell response and generates immunological memory
b cells can take up antigens in a similar manner to other APCs which are presented to t cells via MHC these t cells will already have receptors specific for that antigen and therefore will drive production of memory b cells and plasma b cells
47
explain the basic principles of central tolerance
checkpoints are in place for both t and b cells t cells interact with thymic cortical epithelial cells in the thymus and undergo positive and negative selection. if they self react, they die
48
explain the basic principles of peripheral tolerance
some self reactive b and t cells bypass the central tolerance mechanism and peripheral tolerance will prevent their activation self reactive t cells do not get all three signals from the dendritic cells for activation and differentiation, so if there is loss of signal 2 or 3 then there are anergic t cells or cells targeted for deletion via apoptosis
49
explain the role of plasma factors in the clotting process
the coagulation pathway leads to the production of fibrin, which is the main component of clot formation. the fibrinolytic system uses plasmin to control degradation of fibrin clots balance between these two systems is important
50
in addition to coagulation, what are the other plasma factor cascades and how are they interlinked to support the healing processes and inflammatory responses
kinin fibrinolytic complement coagulation
51
what is the plasma factor that activates all four enzymatic cascades that support healing and inflammation
coagulation factor XII - hagement factor
52
what are the different roles of macrophages in chronic inflammation
M1 macrophages are activated when there is tissue injury by driving an inflammatory response M2 macrophages are involved in tissue repair through suppression of inflammatory responses
53
how can chronic inflammation cause soft tissue destruction
- tissue injury involves activation of coagulation, recruitment of immune cells, production or arachidonic acid metabolites like prostaglandins - tissue repair involves fibrosis, using growth factors to drive cellular recruitment and angiogenesis
54
what molecule functions in reconstructing soft tissue
matrix metalloproteinases
55
describe the phases involved in formation of granulation tissue
first is vascular granulation tissue - proliferating capillaries, fibroblasts and immune cells - new capillaries are leaky which allows cells and fluid to leak into the tissue second is fibrous granulation tissue - capillaries regress and immune cells return to the blood - mature fibroblasts which lay down collagen - collagen is remodelled to an early fibrous scar
56
what are the major causes of cell injury
microbial infection physical agents irritants and corrosive chemicals tissue necrosis
57
how does uv radiation lead to cell injury
dna damage resulting from uv exposure leads to apoptosis via activation of p53 if larger doses of the same injurious agent affect the cell, then necrosis may be the cause of cell death due to coagulation of cellular proteins, disruption of cell membranes and changes to the nucleus
58
what is the principle mechanism of type 1 hypersensitivity, and what are the cells and mediators involved
- allergens processed by APCs - presented to t helper cells - plasma b cells produce IgE - allergen react with IgE and the complexes bind to mast cells and basophils - histamine release
59
what treatments are available for hay fever and how do they work biologically
IgE responses drive mast cells to release histamine, so antihistamines are the logical choice of therapy antagonistic in their actions, block the binding of histamine to the receptors on mast cells and basophils

Pathology and Immunity (16 decks)

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