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Topic 6 Flashcards

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1
Q

What factors can be used to estimate time of death?

A
  • Extent of decomposition
  • Stage of succession
  • Forensic entomology
  • Body temperature
  • Muscle contraction/rigor mortis
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2
Q

What is the extent of decomposition, and how can it be used to estimate time of death?

A
  • Decomposers break down skin over several week by digestive enzymes
  • What stage the body is at presents time since death.
  • Effected by temp and oxygen availability
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3
Q

What is the stage of succession and how can it be used to estimate time of death?

A
  • Changes in type of organisms found on a body over time
  • Bacteria, fly, larvae, beetles
  • Effected by where the body is located and availability of oxygen
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4
Q

What is forensic entomology, how can this be used to estimate time of death?

A
  • Study of colonisation of insects on a body
  • Different insects colonise a body at different times
  • Blowfly are first to colonise
  • Effects are humidity and temperature
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5
Q

How can pathologists use forensic entomology to estimate time of death?

A
  • The number of species present
  • Life cycle stages of insects present
  • Succession of insect species
  • Life cycle is dependent on temperature of environment
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6
Q

What is body temperature and how can this be used to estimate time of death?

A
  • No metabolic reactions occur when dead and the temp should be 37 degrees
  • Body temp decreases by 1-2 degrees each hour
  • Effects are air temp, sa:v ratio, clothing worn
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7
Q

What is rigor mortis, and how can it be used to estimate time of death?

A
  • Muscle contraction within 4-6 hours after death
  • Lactic acid causes pH to fall so inhibits enzymes and ATP no longer produced
  • ATP synthase loses shape of active site so no more muscle contraction and become fixed in position
  • Effects are muscle development and temperature of surroundings.
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8
Q

What happens to muscle cells in rigor mortis?

A
  • No more oxygen reaches cells so respire anaerobically which produces lactic acid.
  • Decreases pH of cells, denaturing enzymes
  • Without ATP muscles become fixed in a contracted state
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9
Q

How useful can body temperature be in providing evidence for time of death?

A
  • Only useful for a short period of time following death
  • Need to know ambient temperature
  • Factors affect temp drop eg. clothing
  • Drop in body temp is algor mortis
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10
Q

How do decomposers break down dead organic matter?

A
  • Secrete enzymes that break large molecules into smaller ones
  • CO2 and methane is produces
  • Released into atmosphere and go through carbon cycle
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11
Q

What are introns vs exons?

A
  • Introns - sections of DNA which do not code for proteins
  • Exons - sections of DNA that code for proteins
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12
Q

What happens in the process of splicing?

A
  • Pre-mRNA non coding intron sections are removed - Coding exons are joined together
  • The resulting mRNA molecule contains only the coding sequences of the gene
  • Forms mature mRNA
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13
Q

What is pre-mRNA?

A
  • The mRNA that has been transcribed with both introns and extons
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14
Q

What is alternative splicing?

A
  • Removing exons so different combinations of mature mRNA are formed.
  • The exons of genes can be joined (spliced) together in many different ways to produce different mature mRNA molecules
  • Therefore different amino acid sequences.
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15
Q

What is splicing catalysed by?

A
  • Enzyme-RNA complex called spliceosome
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16
Q

How can DNA profiles be created?

A
  • Isolating sample of DNA
  • Copies produced using PCR
  • Restriction enzymes to produce DNA fragments
  • Gel electrophoresis of sample
  • Analyse banding pattern of fragments by fluorescent dye/uv
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17
Q

What does PCR require?

A
  • DNA sample to be amplified
  • Primers
  • Taq polymerase
  • Free nucleotides
  • Buffer solution
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18
Q

What are the stages of PCR reaction?

A
  • DNA sample, nucleotides, taq polymerase and primer sequence are mixed
  • Denaturation - thermocycler heated to 95 degrees to break hydrogen bonds so two single strands of DNA
  • Annealing - temp increased to 50-60 degrees so primers bind to 3’ end
  • Elongation - temp increased to 72 degrees so Taq polymerase can synthesise new complementary strands
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19
Q

How does gel electrophoresis work?

A
  • Amplify using PCR
  • Separate using restriction enzymes
  • DNA loading dye is added to PCR tube and DNA fragments are inserted into well of agarose gel plate
  • Electrical current is applied
  • DNA moves to positive anode as it is negatively charged
  • Smaller fragments move faster through gel so mass separates them
  • DNA binding dye is added and UV is shone to compare bands
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20
Q

What is southern blotting?

A
  • DNA profile transferred onto nylon membrane
  • Buffer solution is placed on top.
  • Radioactive probe attaches to band to expose xray paper
  • Increases longevity of DNA profile
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21
Q

How can DNA profiles be compared?

A
  • Total number of bands
  • Position of bands
  • Size/width of bands
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22
Q

What is a DNA profile?

A
  • Specific pattern of DNA bands from an individuals genome
  • Relies on short, repeating sequences of DNA found within non-coding regions of DNA
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23
Q

How does a DNA profile work?

A
  • DNA obtained
  • DNA amplified in PCR
  • DNA separated into fragments using restriction enzymes
  • Gel electrophoresis
  • Southern blotting
  • Fluorescent stain for UV light
  • Analysed and compared
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24
Q

What are STRs?

A
  • Short tandem repeats
  • Short, repeating sequences of DNA
  • Each locus will differ in number of repeats between homologous chromosomes and between individual
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25
Q

How is DNA extracted?

A
  • DNA obtained from tissue samples via mouth, blood, hair, skin
  • Amplified using DNA
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26
Q

What is DNA digestion?

A
  • DNA is digested by cutting into small fragments using restriction endonucleases
  • Endonucleases are an enzyme that cut up DNA at a specific sequence of bases called a recognition sites
  • Cut DNA into fragments but leaves STRs intact
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27
Q

What type of cells are bacteria?

A
  • Prokaryotes
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28
Q

What are the features of a bacterial cell?

A
  • 70s ribosomes
  • Lack of membrane bound organelles
  • Single circular chromosome free in cytoplasm
  • Peptidoglycan cell wall
  • Cell membrane with mesosomes
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29
Q

What is a virus?

A
  • Non-living pathogen
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30
Q

What is the features of a virus?

A
  • Nucleic acid core surrounded by capsid
  • Lipid envelope with proteins attached
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31
Q

What are the differences between structure of bacteria and viruses?

A
  • Bacteria DNA is circular/Viral DNA is linear
  • Bacteria have ribosomes/Viruses do not
  • Bacteria are cells/Viruses are not
  • Bacteria has cell wall/Viruses have protein capsid
  • Bacteria have DNA/ Viruses have RNA or DNA
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32
Q

How do viruses reproduce?

A
  • Replicate in living host cells they infect
  • Hijack protein production machinery and cause lysis and kill the cell and build new virus particles
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33
Q

What is a disease?

A
  • An illness or disorder to the mind/body leading to poor health
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34
Q

What is an infectious disease?

A
  • Disease caused by pathogens which are transmissible and can be spread in population
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35
Q

How is TB spread?

A
  • Through inhalation of droplets from a person infected by TB
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36
Q

What bacteria causes TB?

A
  • Mycobacterium tuberculosis
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37
Q

How does TB cause illness?

A
  • TB bacteria is engulfed by phagocytes
  • Bacteria is reproduced when inside phagocytes and over time those infected become encased in tubercles in the lungs where it remains dormant
  • When it is activated it overpowers immune system and creates a lesion (granuloma) so damages tissue and cause organ failure
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38
Q

What is primary TB?

A
  • Infects lungs cause fatigue, fever, coughing, weight loss
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39
Q

What is secondary TB?

A
  • Immunocompromised individual
  • Produces extensive damage to respiratory system
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40
Q

Why do dormant TB not get destroyed by the immune system?

A
  • Bacteria hides inside macrophages
  • Thick waxy cell wall
  • Lysosomes cannot fuse with phagocytotic vacuole
  • Bacteria within tubercles cannot be destroyed
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41
Q

How does HIV infect human cells?

A
  • GP120 on HIV attaches to CD4 receptors on T helper cells
  • Allows HIV to enter host cells
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42
Q

How does HIV replicate once in blood?

A
  • GP120 glycoproteins attach to CD4 receptors on T helper cells
  • Capsid fuses with T helper cell membrane, releasing RNA
  • Reverse transcriptase converts viral RNA into DNA then integrates the viral DNA into the cell DNA.
  • Transcribed to generate mRNA which encodes HIV viral proteins, leading T helper cells to infect more T cells
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43
Q

What is HIV?

A
  • Two single-stranded RNA retrovirus
  • Containing enzyme reverse transcriptase
  • Has attachment proteins embedded in lipid envelope.
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44
Q

What happens without T helper cells?

A
  • Cytotoxic T cells can’t kill infected cells
  • Specific antibodies cannot be produced
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45
Q

How does HIV lead to AIDS?

A
  • After initial infection, replication rates drop (latency period)
  • Virus reduces number of T helper cells
  • B cells no longer activated so no antibodies are produced
  • Decreased ability to fight diseases so weakens immune system
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46
Q

How do anti viral drugs work in the treatment of HIV?

A
  • Drugs prevent viral replication
  • Inhibit reverse transcriptase so viral DNA cannot be formed from viral RNA
  • Inhibit integrase so viral DNA cannot integrate
  • T helper cells will not be killed
47
Q

What are the evasion mechanisms of HIV?

A
  • Virus kills helper T cells reducing number of cells that could be detected
  • Antigenic variability due to high mutation rate
  • Infected cells don’t produce APCs so WBCs do not recognise and destroy infected cells
48
Q

Why does AIDs lead to death?

A
  • No longer any antibodies against pathogens
  • Immunocompromised so unable to fight infections
49
Q

What factors increase rate of progression into AIDs?

A
  • Access to healthcare
  • Age
  • Number of infections
  • Strain
50
Q

What is the correlation of HIV and TB?

A
  • Dormant TB may become an active infection when immune system weakened
  • HIV causes immunodeficiency
51
Q

What is an infection?

A
  • When a pathogen gets inside human tissues or cells
52
Q

What are the barriers to infection on the human body?

A
  • Skin: physical barrier to infection
  • Skin and Gut flora: microorganisms which compete with pathogens
  • Stomach acid: HCL creates high pH (acidic) environment
  • Lysozyme: Kills bacteria by breaking down cell wall causing lysis
53
Q

How does flora protect the body from infection?

A
  • Better adapted to conditions
  • Prevents growth of microorganisms by providing competition
  • Releases chemicals/toxins
54
Q

What is the non-specific immune response?

A
  • When a body defends itself against a pathogen but the response is not specific to pathogen
  • Eg. phagocytosis, inflammation
55
Q

How does bacteria cause a specific immune response?

A
  • Bacteria engulfed by macrophages
  • Antigen presenting cell produced
  • T helper cells with complementary CD4 bind to APC
  • Cytokine released causing cloning of B cells
  • Plasma cells produce antibodies
56
Q

How does inflammation work?

A
  • Swelling of a tissue caused by infection to destroy invading pathogen
  • Mast cells release Histamine
  • Causes vasodilation to increase blood flow
  • Increases permeability of capillaries to allow blood plasma to enter tissue
57
Q

How do interferons work?

A
  • Anti-viral proteins produced in infected cells which diffuse to surrounding cells
  • Inhibits viral replication and microbial protein synthesis
  • Activates WBCs involved in specific immune response
58
Q

How does interferon respond to infection by viruses?

A
  • Interferon prevents virus attaching to uninfected host cells by binding to receptors
  • This therefore prevents the virus entering the cell
  • Viruses cannot replicate and infect more cells
59
Q

How does phagocytosis work?

A
  • Phagocyte recognises pathogen as non self from the foreign marker (antigen)
  • Phagocyte engulfs pathogen to form a phagosome (vacuole) by endocytosis
  • Pathogen is broken down by enzymes (phagolysosome)
60
Q

How does a macrophage ingest bacteria?

A
  • By phagocytosis
  • Bacteria enclosed inside a phagosome
  • Bacteria is broken down by enzymes
  • Present antigens on membrane (antigen-presentation)
61
Q

What are phagocytes?

A
  • Macrophages + neutrophils
62
Q

What are antigen representing cells?

A
  • Phagocytes engulf antigens which are then presented on cell surface membrane of antigen presenting cells
  • Lymphocytes with receptors that are specific to antigens bind to APC.
63
Q

What are self vs non self antigens?

A
  • Self = antigens produced by organisms own body cells, do not stimulate immune response
  • Non self = antigens not produced by organisms own body cells, stimulate immune response
64
Q

What happens when a pathogen first infects tissue?

A
  • Neutrophils arrive first and each engulfs 5-20 pathogenic cells
  • Macrophages then arrive and engulf 100s of pathogenic cells
65
Q

What are antigens?

A
  • Markers on the cell surface which allow cell recognition
  • Trigger immune response
66
Q

How do antibodies disable pathogens?

A
  • Bind to pathogen receptors to prevent pathogens infecting host cells
  • Act as anti toxins by binding to toxins produced by pathogens
  • Pathogens clump together (agglutination) so they can’t spread
67
Q

What are antibody binding sites?

A
  • They have specific shapes which makes them complementary to specific target antigens
68
Q

What is the structure of antibodies?

A
  • 4 polypeptide chains: 2 heavy chains, 2 light chains
  • Y shaped structure
  • Has a constant and variable chain
69
Q

What is the constant region?

A
  • Heavy chain
  • No not vary within class of antibody
  • Bind to all immune cell receptors
70
Q

What is the variable region?

A
  • Short chain
  • Amino acid sequence is different on each antibody
  • Bind to antigen to form antibody-antigen complex
71
Q

What is the importance of the end of a variable region on the end of an antibody?

A
  • It is the antigen binding site
  • Gives antibody specificity for binding to the antigen
72
Q

How are membrane bound antibodies different from those secreted into the blood?

A
  • Membrane bound antibodies are attached to the surface of lymphocytes.
  • In non bound antibodies, gene can undergo alternative splicing to remove extra section for attachment
73
Q

What is the role of an antibody?

A
  • Helps immune cells destroy pathogens
  • Variable region binds to antigen forming antibody-antigen complex
  • Constant region then binds to opsonin receptor on phagocyte
74
Q

How do antibodies work?

A
  • Antibodies have two binding sites
  • Work by agglutination which cause pathogens to clump together
  • For macrophage or neutrophils to engulf and destruct pathogens carrying the antigens (phagocytosis).
75
Q

What is neutralisation?

A
  • Antibodies bind to toxins released by pathogens
  • Prevents toxins damaging
76
Q

What is the primary immune response?

A
  • The body’s initial response to the first time an antigen is encountered by the immune system
77
Q

What is the secondary immune response?

A
  • When the immune system encounters an antigen it has already been exposed to
78
Q

Why does the primary response take a longer time?

A
  • T and B cells have to be activated which takes time
  • Plasma cells need to develop before antigen production begins
79
Q

Why is the secondary immune response stronger and faster?

A
  • Memory cells are present
  • Antibodies are produced more quickly
  • Eliminates pathogens before symptoms appear
80
Q

What is active immunity?

A
  • When antibodies are produced by own immune system
81
Q

What is passive immunity?

A
  • When specific antibodies are introduced from an outside source
82
Q

What is natural vs artificial?

A
  • Natural = natural process
  • Artificial = Introduced
83
Q

What are the two types of active immunity?

A
  • Natural - pathogen exposure
  • Artificial - vaccination
84
Q

What are the two types of passive immunity?

A
  • Natural - breast milk
  • Artificial - transfusion of antibodies
85
Q

What is produced in non-specific immunity?

A
  • Macrophages + Neutrophils
  • Recognise non-self pathogens and destroy by phagocytosis
86
Q

What is produced in specific immunity?

A
  • T lymphocytes + B lymphocytes
  • Recognise specific antigens to produce an immune response
87
Q

Where are T cells produced and where do they mature?

A
  • Produced in bone marrow
  • Mature in thymus
88
Q

What do T cells have?

A
  • Specific cell surface receptors (T cell receptors)
89
Q

How are T cells activated?

A
  • They bind to their specific antigen on the surface of an antigen presenting cell
  • Shapes are complementary
  • Called clonal selection
90
Q

What is direct contact?

A
  • Lymphocyte comes across pathogenic cell
91
Q

What is indirect contact?

A
  • Lymphocyte comes across APC which phagocytosed the pathogen
92
Q

What is the process of cell mediated response?

A
  • Phagocytosis by phagocytes
  • Macrophages present antigen-presenting cells to T helper cells
  • T cells release cytokines to trigger T killer cells
  • Stimulate phagocytic cells, such as macrophages and neutrophils to engulf non-self pathogens.
93
Q

What do T cells differentiate into?

A
  • T killer cells - destroy own body cells infected by pathogens, display APC
  • T helper cells - release cytokines to stimulate B cells to produce antibodies
  • T memory cells - remain in blood enabling a secondary immune response
  • T regulatory cells - inhibit immune response once pathogens destroyed so own body cells aren’t destroyed
94
Q

What is the process of the humoral response?

A
  • Phagocytosis by phagocytes
  • Macrophages present antigen-presenting cells to T helper cells
  • T cells release cytokines for B cell activation
  • B cells form clones and differentiate into Plasma cells
  • Produce memory cells
95
Q

Where do B cells divide and mature?

A
  • Bone marrow
96
Q

How are B cells activated?

A
  • B cell binds to antigen forming antigen-antibody complex. (APC)
  • T helper cell binds to B cells and T helper cells releases cytokines to activate the B cell.
97
Q

What do B cells differentiate into?

A
  • Plasma cells - secrete antibodies into blood
  • B memory cells - remain in blood to enable secondary immune response when same antigen is encountered
98
Q

What is the role of antigen-presentation in body’s specific immune response to infection?

A
  • Macrophages present antigen to T helper cells.
  • Activates T killer and B cells
  • B cells act as an antigen-presenting cell
  • Result in plasma cells to produce antibodies
  • T killer cells destroy infected host cells
99
Q

What is a vaccine?

A
  • Dead/weakened pathogens injected into the body
  • Artificial active immunity
  • Produce memory cells for strong immune response
100
Q

What is the evolutionary race between pathogens and hosts?

A
  • When one evolves, another catches up
  • Pathogens evolve new methods to overcome the immune system.
101
Q

How does the evolutionary race affect antigen presentation to T helper cells?

A
  • Mutation occurs in bacterial DNA, changes APC
  • Memory T cells will not recognise antigen
  • Another primary immune response to activate more T helper cells
102
Q

What is a selection pressure?

A
  • External factor which affects organisms ability to survive
103
Q

What is antigenic variation?

A
  • Pathogens have resistant mechanisms
  • Frequent pathogen mutations
  • Vaccines no longer effective as antigens are no longer recognised
104
Q

What is vertical evolution?

A
  • Bacteria passing adv. allele from one generation to next
105
Q

What is horizontal evolution?

A
  • If adv. allele is passed from one bacteria to next but no change
106
Q

Why might a vaccine be given to immediate family/health workers despite clinical trials being incomplete?

A
  • Disease may be fatal
  • Risk of disease is worse than risk from vaccine
  • Very close contact
  • Helps to reduce spread
107
Q

What are the two types of antibiotics?

A
  • Bactericidal - kills bacterial cells
  • Bacteriostatic - Inhibits growth/multiplication
108
Q

What are some of the mechanisms antibiotics use to disrupt bacterial cell growth?

A
  • Inhibit bacterial wall synthesis
  • Inhibit protein synthesis
  • Damage cell membranes
  • Inhibit nucleic acid synthesis
109
Q

What is MRSA?

A
  • Multiple resistant bacteria found in hospitals
110
Q

What measures do hospitals have in place to reduce the spread of viruses?

A
  • Regularly wash hands
  • Isolation ward
  • Surfaces should be disinfected
  • No ties, watches, sleeves
111
Q

What is the risk of antibiotic resistance?

A
  • Difficult to treat as do not respond to regular antibiotics
  • Cause serious health complications
112
Q

What hospital practices have been developed to reduce the risk of antibiotic resistant bacteria?

A
  • No antibiotic prescriptions for minor infections/diseases
  • rotate the use of different antibiotics
  • prescription of a narrow spectrum antibiotic to treat the infection
113
Q

How does antibiotic resistance in bacteria arise?

A
  • Random mutation in an individual
  • Resistant survives and passes on mutation via binary fission
  • Increases in frequency in the population

A Biology A Level (8 decks)

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