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A Level Biology (SNAB) > Topic 6 > Flashcards

Topic 6 Flashcards

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1
Q

Microorganisms

A
  • Decompose organic matter
  • respire -> releasing CH4 + CO2 (carbon cycle)
  • in and on animals/plants, which die and the microorganisms then secrete enzymes to break them down
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2
Q

Steps to Estimating time of death

A
  1. Body temperature
  2. Degree of muscle contraction
  3. Forensic entomology
  4. Extent of decomposition
  5. Stage of succession
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3
Q

Time of Death: Body temperature

A

Heat produce form metabolic reactions in mammals
- humans = 37 C
TOD: metabolic relations slow down -> stop
- body temp fall -> equals surroundings = Algor Mortis
- human body cools at 1.5 C to 2.0 C per hour
-> cooling rate affected by: air temp, body weight, clothing, position

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4
Q

Algor Mortis

A

The process in which the body temperature falls, after time of death, to equal that of its surroundings (at an estimated rate of 1.5 to 2.0 C per hour)

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5
Q

Time of Death: Degree of Muscle Contraction

A

4-6 hrs after death -> contract & become stiff = Rigor Mortis

  • muscle cells deprived of oxygen
  • respiration still occurs -> anaerobic -> lactic acids builds up in muscle
  • pH of cells decreases -> inhibits ATP producing enzymes
  • No ATP -> myosin + actin bonds in muscle cells become fixed -> stiffen
  • – smaller muscles in head contract first
  • – large muscles in lower body = last
  • 12-18hrs after TOD = every muscle contracted
  • 24-36 hrs after TOD = wears off
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6
Q

Rigor Mortis

A

The process in which the body’s muscles begin to contract & become stiff 4-6 hrs after TOD.

  • affected by:
  • -degree of muscle development (less = faster)
    • temperature (higher = faster)
  • 12-18hrs after TOD = every muscle contracted
  • 24-36 hrs after TOD = wears off
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7
Q

Time of Death: Forensic Entomology

A

Study of the insect colony present at TOD

  • estimated by identifying type of insect present
    • flies = few hrs after death
    • beetles = later
  • Stage of life cycle:
    • blowfly larvae: hatch from egg 24 hrs after laid

Conditions that can affect life cycle:

  • drugs
  • humidity
  • oxygen
  • temperature
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8
Q

Blowfly larvae lifecyle

A

ngng

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9
Q

Time of Death: Extent of Decomposition

A

Bacteria + enzymes start to decompose

  1. hrs to a few days: cell + tissue breakdown
    - skin = greenish hue (Putrefaction)
  2. few days to a week: microorganisms decompose tissues
    - gases produced (methane) -> body bloats
    - skin blisters & falls off
  3. few weeks: tissues begin to liquify
    - seep into area around body
  4. few months -> years: skeleton
  5. decades -> centuries: skeleton begins to disintegrate

note: affected by temperature + O2 availability
- e.g acidic peat bogs = preserve

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10
Q

Time of Death: Stages of Succession

A

Above ground, at TOD:

  1. favourable for bacteria -> decompose tissues
  2. flies & larvae -> fly larvae feed
  3. beetles suited
  4. dead body dries out -> flies leave, beetles remain to decompose
  5. no tissue -> (mostly) no organisms

note: for plants -> insects remain from stage to stage

location: sealed away = no insects
under water = fish / rodents etc

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11
Q

DNA profile

A

Unique genetic fingerprint (except for monozygotic twins)

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12
Q

DNA profile (PCR process)

A
  1. DNA sample taken (blood, saliva, epithelial cells)
  2. Acquisition: DNA separated from sample
  3. Replication: Polymerase Chain Reaction
  4. Separation: Gel Electrophoresis
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13
Q

Fingerprints

A

Types:

  • arch
  • tented arch
  • whorl
  • loop

Sweat + oil secretions placed into iron flakes then computerised

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14
Q

Dental Records

A

Teeth + filings decay slowly -> more resistant to burning

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15
Q

Surgical Implants

A

Recorded number on item that can be linked to surgery

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16
Q

DNA profile: Aquisition

A

DNA broken down in buffer solution

  • small suspended particles separated via filitration/centrifuging
  • Protease enzymes incubated with suspension -> removes proteins
  • Cold ethanol added -> precipitate out DNA
  • continuous washing of DNA with buffer
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17
Q

DNA profile: Restriction Endonucleosis

A

Enzyme = EcoRI

  • cuts DNA out at specefic base sequences (4-6 bases long)
  • cuts between G & A bases when ‘GAATC’ sequence occurs
  • if the restriction site is either side of short tandem repeats, DNA fragment remains intact, but cut from rest of genome
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18
Q

DNA profile: Polymerase Chain Reaction

A

Uses DNA primers, which are marked with fluorescent tags

  • DNA placed in reaction tube with DNA polymerase, primers & nucleotides
  • once in PCR machine, undergoes temperature change cycle:
    1. 95 C = separates double stranded DNA (breaks H bonds)
    2. 55 C = optimises annealing of primer to target DNA sequence (start of STR), then polymerase attaches & replication occurs
    3. 70 C = optimum for heat stable DNA polymerase
  • > lines up free DNA nucleotides along each template strand (complementary strand formed)
  • > two new copies of DNA fragment

Cycle starts again, using all copies of DNA fragment (each cycle doubles DNA)

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19
Q

DNA profile: Gel Electrophoresis

A

Separates fragments according to length

  1. DNA placed on agrose/polyacrylamide gel (in wells)
    - provides a stable medium through which the fragments move
  2. Gel is submerged in a buffer solution
  3. Connected to electrodes which provide a potential difference across the gel
    - -ve fragments migrate through the gel according to overall charge + size (smaller + less repeats = faster)
    - smaller fragments end up closer to +ve electrode
  4. reference sample with fragments of known length may be added to the gel = DNA ladder/marker
  5. fragment lengths are measured in base pairs
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20
Q

DNA profile: Southern Blotting

A

Gel placed directly onto nylon/nitrocellulose membrane, with wad of fry absorbent paper placed on top

  • > acts as a wick to draw buffer solution up through the gel (carrying DNA fragments) onto the membrane
  • fragments maintain position relative to each other
  • denatured into single strands -> exposing base sequence
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21
Q

Buffer solution (DNA profiling)

A

Detergent + Salt that disrupts cell membrane

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22
Q

Introns

A

Non-coding regions in DNA

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23
Q

Exons

A

Coding regions in DNA

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24
Q

Short Tandem Repeats (STR)

A

Sequences of repeated bases

  • 2 to 50 pairs, 5 to several hundred times
  • same locus on homologous chromosome pairs
  • STR quantities differ between individuals, this difference = identifier
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25
Q

DNA profile: Probe attachment + viewing (fluorescent or radioacitve

A

Nylon/nitrocellulose membrane incubated with excess of a labelled DNA probe

  • allowing time for probe to bind to any complementary sequences (hybridising)
  • > unbound probe washed away

If probe = radioactive (or labelled with radioactive phosphorous(

  • membrane -> dried
  • placed next to x-ray film -> blackens wherever probe has bound with DNA

If probe = fluorescent
- visualised on membrane under UV light

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26
Q

Radioactive Phosphorus

A

32^P

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27
Q

Labelled DNA Probe

A

Short section of DNA with a base sequence complementary to the target DNA sequence that needs to be located

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28
Q

DNA profile (Restiction endonucleosis process)

A
  1. DNA sample taken (blood, saliva, epithelial cells)
  2. Restriction Endonucleosis
  3. Gel Electrophoresis
  4. Southern Blotting
  5. Probing + visualisation
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29
Q

DNA profile: PCR analysis using Gel Electrophoresis

A

As DNA primers have fluorescent tags, the normal gel electrophoresis occurs, but then the system can be automated

  • as DNA fragments move through gel, they pass a laser
  • the dye in the tag fluoresces -> light detected
  • gives the time taken for fragment to pass through gel
  • > calibrated against known fragment lengths (determined by no. of base pairs)

Note: several STR loci can be analysed at once using tags that fluoresce at different wavelengths

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30
Q

Bacteria Structure (with diagram)

A

Single Celled prokaryotes
- few micrometers
(insert diagram)

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31
Q

Virus Structure (with diagram)

A
  • Nucleic acids surrounded by proteins
  • tiny (decimal of micrometers)
  • Nucleic acid core (DNA or RNA)
  • some carry proteins inside their capsid
  • some have an envelope
  • Attachment proteins
    (insert diagram)
32
Q

Virus’ Envelope

A

A stolen cell membrane from a previous host cell

33
Q

Virus’ Capsid

A

A protein coat around the virus’s core

34
Q

Virus’ Attachment proteins

A

Proteins that stick out from the capsid or envelope, and allow the virus to cling to a suitable host cell

35
Q

Pathogens

A

Any organism that causes infectious diseases

e.g. some bacteria, some fungi, all viruses

36
Q

HIV

A

Human Immunodeficiency Virus

  • infects + destroys T helper cells
  • uses them as host cells
  • T helper cells usually activate other immune system cells
37
Q

AIDS

A

Acquired Immune Deficiency Syndrome

38
Q

HIV infection pathway (applicable to other viruses)

A
  1. Spread via infected bodily fluids
    - contact MUCOSAL surfaces (genital tissue), damaged tissue, or is injected into bloodstream
  2. (all viruses) reproduces inside cells of infected organism e.g. T-Helper cells (needs enzymes + ribosomes to replicate)
    - attachment proteins attach to receptor molecule (on cell membrane)
    - Capsid is inserted into cell, uncoats & releases RNA into cytoplasm
    - reverse transcriptase used to make complementary strand of DNA from viral RNA template
    - > double -stranded DNA -> inserted into human DNA
    - host-cell enzymes make viral proteins (using viral DNA)
    - viral proteins -> new viruses
    - > bud from cell -> infect others
39
Q

HIV initial infection & latency period

A

II: HIV replicates rapidly -> severe flu like symptoms
LP: HIV replication drops -> no symptoms; can last for several years

40
Q

AIDS development

A

HIV infection eventually leads to AIDS = immune system deteriorates -> eventually fails (takes roughly 10 years to develop)

Classified as having AIDS when:

  • Symptoms of failing Immune start to appear
  • T helper cell count drops below certain level
  • > leads to opportunistic infections

Symptom sequence:

  1. Minor infections of mucus membranes & recurring respirator infections (lower T helper count)
  2. AIDS progresses -> T helper count drops further
    - > more serious infections:
    - chronic diarrohea
    - severe bacterial infections
    - tuberculosis
  3. Late stages = v.low T helper count
    - > serious infections
    - toxoplasmosis of the brain (parasite)
    - candidiasis of the respiratory system (fungal)
    - > causes death (secondary infection)
41
Q

Tuberculosis infection pathway

A

Mycobacterium Tuberculosis causes TB

  1. droplets (tiny) inhaled into lungs
  2. bacteria taken up by phagocyte (wbc) in lungs (inhaled)
  3. bacteria replicate in phagocyte
  4. infected phagocytes -> sealed in tubercles (structures in lungs)
  5. bacteria -> dormant (no obvious symptoms)
  6. dormant bacteria -> reactivate -> overcome immune system -> TB
    - more likely in weakened immune systems (e.g. AIDS)
    - length of time between infection -> TB varies (weeks to years)
42
Q

TB sequence of Symptoms

A
  1. fever, general weakness, severe coughing (lung inflammation) = initial
  2. progresses -> damages lungs -> (untreated) respiratory failure -> death
  3. can spread e.g. brains + kidneys
    - untreated -> organ failure -> death
43
Q

Pathogen routes (of infection)

A
  • cuts in skin
  • digestive system (contaminated food + drink)
  • respiratory system (droplet inhalation)
  • mucosal surfaces (nose, mouth, genitals)
44
Q

Barriers to prevent infection

A
  1. Stomach acid = acidic conditions -> kill
    - some pass into intestines -> invade gut wall cells
  2. Skin = physical barrier
    - blood clots extend protection
    - margin to enter
  3. Gut + skin flora = billions of harmless microorganisms
    - compete with pathogens for nutrients + space
  4. Lysozymes = enzyme (kills bacteria by damaging cell wall)
    - mucosal surfaces -> secretions = contain lysozyme
45
Q

Foreign antigens ->

A

Trigger immune response
1. non specific
or
2. specific

46
Q

Antigen

A

molecules found on cell surface

47
Q

Non-specific immune response (stages)

A

Happens in the same way for all microorganisms , and occurs straight away:

  1. Inflammation at infection site
  2. Production of Interferons
  3. Phogocytosis + Lysozyme action
48
Q

Inflammation at infection site: Non-specific immune response

A
  1. immune system cells recognise foreign antigens
    - > release histomine molecules (trigger inflammation)
  2. Triggers vasodilation; increasing blood flow around infection site
  3. Also increases permeability of blood vessels
  4. immune system cells flood to site
    - due to increased permeability -> move into infected tissue
  5. start to destroy pathogen
49
Q

Production of interferons: Non-specific immune response

A
  • cells infected by virus -> produce interferons
  • > prevent virus spreading to other cells
  1. prevent viral replication
    - inhibit production of viral proteins
  2. Activate cells involved in specific immune response
    - kills infected cells
  3. Activate other Non-specific immune responses
    - e.g. promote inflammation
50
Q

Interferons

A

Anti-viral proteins

51
Q

Phagocytosis + Lysozyme action: Non-specific immune response

A
  1. Phagocyte recognises pathogens antigens
  2. Cytoplasm moves around pathogen -> engulfs it
  3. Pathogen contained in phagocytic vacuole
  4. Lysosyme fuses with phagocytic vacuole
    - lysozyme breaks pathogen down
  5. Phagocyte presents pathogens antigens
    - sticks antigens on surface to activate other immune system cells
    - antigen presenting cell
52
Q

Specific Immune response (brief)

A

Antigen Specific (occurs after non-specific if necessary)

  1. Phagocytes activate T Cells
  2. T helper cells activate B cells
53
Q

Phagocytes activate T Cells: Specific Immune response

A

T cell = white blood cell

  • surface covered in receptors
  • receptors bind to antigens
  • > displayed by antigen presenting cells (macrophages; type of phagocyte)
  • each T cell = different shaped surface receptors
  • receptor + complimentary antigen -> bind
  • > activate T Cell -> divides to clone

Different T cells = different functions:

  1. T helper = substance released to activate
    - B Cells
    - T killer cells
    - macrophages
  2. T-Killer = attach to antigen of infected cell -> kill cell
  3. T-memory
54
Q

T Helper cells activate B Cells: Specific Immune response

A

B cells = white blood cells

  • covered by proteins = antibodies
  • each B cell = different shaped antibodies
  • antibodies + antigens = antigen-antibody complex
  • antibody + complimentry antigen -> bind
  • binding + substances form T helper cells -> activates B cells

B cell activated -> divides (mitosis) to form:

  • plasma cells = B effector cells
  • B memory cells
55
Q

Plasma Cells

A

= B cell clones

-> secrete antibodies

56
Q

Antibodies (structure)

A
  1. 4 polypeptide chains
    - 2 heavy
    - 2 light
    - each chain has a variable + constant region
  2. variable regions = antigen binding site (complementary shape)
  3. hinge region = provides flexibility (accommodates binding)
  4. constant region = allows for binding to receptors on immune system cells
    - same on all antibodies
  5. Disulphide bridges = hold chains together
57
Q

Antibodies (Structural diagram)

A

Insert Image

58
Q

How antibodies clear infection

A
  1. Agglutinate pathogens
    - antibodies = 2 binding sites -> 2 pathogens at a time (clump together)
    - phagocytes bind to antibodies -> phagocytoses clump
  2. Neutralising toxins
    - bind to toxins, inhibiting effect (neutralised)
    - entire complex phagocytosed
  3. Prevent pathogen binding to human cells
    - antibody binds to antigen
    - block cell surface receptors needed to bind to host cell
    - pathogen cannot attach -> prevents infection
59
Q

Types of antibodies

A
  1. Membrane bound

2. Secreted

60
Q

Membrane bound antibodies

A

Attached to B cell membrane

  • extra protein section on the heavy chains to anchor to membrane
  • > copied into mRNA; protein synthesised, but modified before translation to provide a different heavy chain for secreted vs membrane bound antibodies (more than one protein from same gene)
61
Q

Secreted antibodies

A

Free floating (come from plasma)

  • heavy chain coded for by a single gene
  • > copied into mRNA; protein synthesised, but modified before translation to provide a different heavy chain for secreted vs membrane bound antibodies (more than one protein from same gene)
62
Q

mRNA modified before translation because…

A
  1. genes contain sections that do not code for amino acids (introns)
  2. Transcription = exons + introns copied into mRNA
    = pre-mRNA
  3. Introns removed = splicing
    - exons joined -> mRNA strands
    - occurs in Nucleus
    = post-transcriptial change
  4. Sometimes exons are also removed
    - different mRNA strands = alternative splicing (possible for around 95% of genes)
    - allows for more more than one sequence -.> multiple proteins possible from 1 gee=ne
63
Q

Memory Cells

A
  1. Pathogen enters body 1st time -> antigens activate immune system
    - NSI -> SI response = primary response; slow as few B cells for antibodies
    - enough antibodies produced -> infection overcome (symptoms)
  2. After exposure, T + B cells produce memory cells
    - remain in body
    - T memory remember specific antigen
    - B memory record antibody recquired
    = immune (able to respond quickly)
  3. 2nd pathogen exposure
    - > quicker + stronger response = secondary response
    - T memory cells divide into correct T cell type to kill antigen carrying cell
    - B memory cells divide into B effector cells to produce antibodies (few/no symptoms)
64
Q

Types of Immunity

A

Active:

  1. Natural = Catch a disease
  2. Artificial = Vaccine

Passive:

  1. Natural = baby receives antibodies from mother (placenta + milk)
  2. Artificial = injected with antibodies (e.g. tetanus shot)
65
Q

Active Immunity

A

Organisms own immune system makes antibodies after being stimulated by an antigen

66
Q

Passive Immunity

A

Antibodies made by a different organism are provided, allowing for short-term, immediate immunity

67
Q

Primary/Secondary immune response diagram

A

Insert diagram

68
Q

Vaccines

A

Contain antigens -> stimulate primary response
- no disease
- leads to immunity
Protect (usually) against different strains
- caused by antigenic variation

69
Q

HIV’s Evasion mechanism

A
  1. Kill infected immune system cell
    - reduced cell no. -> reduces detection
  2. HIV = high mutation rate in genes coding for antigens
    - change antigen structure = Antigenic Variation
    - > primary response for each new strain
  3. Disrupts antigen presentation in infected cells
    - prevents recognising + killing
70
Q

Mycobacterium Tuberculosis evasion mechanism

A
  1. Engulfed by phagocyte -> produces substance
    - prevents lysosyme fusing with phagocytic vacuole
    - bacteria not broken down
    - continues multiplying undetected
  2. Disrupts antigen presentation
    - stops recognising + killing
71
Q

Types of Antibiotics

A
  1. Bacteriocidal

2. Bacteriostatic

72
Q

Bacteriocidal Antibiotics

A

Inhibits enzymes required tom make chemical bonds in cell walls

  • prevents growth -> cell death
  • weakens cell wall + pressure (water via osmosis_
  • > bursts
73
Q

Bacteriostatic Antibiotics

A

Inhibit protein production by binding to bacterial ribosomes -> no enzymes
- stops metabolic processes (e.g. growth)

74
Q

Antibiotics

A

Chemicals that affect metabolic processes (such as growth) of bacteria, and can cause their destruction

75
Q

HATs

A

Hospital Acquired Infections
- Patients being treated in hospital more likely to receive them due to traffic, other patients & weakened immune systems

Transmitted Via poor hygiene

  • non-contained coughs/sneezes
  • surfaces not regularly disinfected
  • no hand washing
76
Q

HATs treatment/containing

A

People with HATs moved to isolated ward (reduces likelihood of transmission)

Some HATs = antibiotic resistant, so to prevent + control spread:

  • no antibiotics for minor or viral infections
  • no preventative antibiotics
  • yes to narrow spectrum antibiotics
  • yes to rotating use of different antibiotics
  • courses must be completed (otherwise increases likelihood of resistance)

A Level Biology (SNAB) (10 decks)

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