Biology Topic 6 Flashcards

(33 cards)

1
Q

How do microorganisms decompose organic matter?

A

Microorganisms e.g. fungi and bacteria in and on dead organism secrete enzymes that decomposed the dead into small molecules they can respire, releasing CO2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can body temp he used to measure time of death?

A

All mammals produce heat from metabolic reactions.

From time of death metabolic reaction slow down and eventually stop, causing temperature to fall until it is equal to surroundings temperature.
Scientists know human bodies cool at rate about 1.5-2 degrees per hour. E.g. corpse with temp 35 degrees probably dead for about hour.

Air temp, clothing and body weight affect cooling rate of body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can degree of muscle contraction be used to estimate time of death?

A

4-6 hours after death, muscles in corpse contract and become stiff - this is called rigor mortis.

  1. Rigor mortis begins when muscle cells become deprived of O2.
  2. Respiration had to be anaerobic, causing a build up of lactic acid in the muscle.
  3. The pH of the cells decreases due to the lactic acid, inhibiting enzymes that produce ATP.
  4. No ATP means the bonds between myosin and actin become fixed and the body stiffens.

Rigot mortis is affected by degree of muscle development and temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can forensic entomology be used to estimate time of death?

A
  1. When someone dies body quickly colonised by variety of insects- the study of this is called forensic entomology.
  2. Time of death can be estimated by type of insect on body. E.g. flies often first to appear.
  3. Time of death can also be estimated by stage of life cycle of insect. E.g. blowfly larvae hatch 24 hours after being laid. If only blowfly eggs found you can estimate time of death was less than 24 hours ago.

Drugs, oxygen, humidity and temperature will affect life cycle of insect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can extent of decomposition be used to estimate time of death?

A

Immediately after death bacteria amd enzymes begin to decompose the body.

Hours to few days: skin on body greenish colour.

Few days to few weeks: microorganisms decompose tissues and organs. This produces gases that causes the body to bloat. Skin blisters and falls off.

A few weeks: tissues liquefy and seep out

Months to years : skeleton

Centuries: skeleton disintegrates until nothing left of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can stage of succession be used to.estimate time of death?

A

Types of organism found in a body change over time, going through number of stages of succession.

  1. Immediately after death conditions favourable for bacteria.
  2. As bacteria decompose tissues, conditions become favourable for flies and their larvae.
  3. When fly larvae feed on body conditions become favourable for beetles.
  4. As body dries less favourable for flies, beetles remain as they decompose dry tissues.
  5. When no tissues remain, conditions not favourable for any organisms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What has to be done to make a DNA profile before gel electrophoresis?

A
  1. Obtain DNA sample e.g. from blood or saliva.
  2. PCR
    a. Reaction mixture set up containing DNA sample, free nucleotides, primers and DNA polymerase.

b. Denaturation: heat to 90 degrees to break hydrogen bonds in DNA strands.

c. Annealing : cooled to 50 degrees so primers can bind (anneal) to strands.

d. Extension: heated to 70 degrees so DNA polymerase is at optimum temp.

e. Two new copies made of DNA formed. Cycle repeats. Every PCR doubles the amount of DNA.

  1. Fluorescent tag added so DNA profile can be viewed under UV after gel electrophoresis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe gel electrophoresis.

A

Used to separate fragments of DNA according to their length.

  1. DNA played into a well on a rank loaded with agarose gel.
  2. Electrical current passed through the gel. DNA fragments are negatively charged so move towards anode at far end of the gel.
  3. Short DNA fragments move faster and travel further through the gel. So DNA fragments separate according to length.
  4. Gel is viewed under UV. The DNA fragments appear as bands under UV light. This is the DNA profile.
  5. Two profiles can be compared. More similar = more closely genetically related.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does HIV replicate?

A
  1. Attachment protein attaches to a receptor molecule on the cell membrane of the host T helper cell.
  2. The capsule is released into the cell, where it uncoated and releases genetic material (RNA) into the cell’s cytoplasm.
  3. Inside the cell, reverse transcriptase is used to make a complementary strand of DNA from the viral RNA template.
  4. From this, double-stranded DNA is made and inserted into human DNA.
  5. Host cell enzymes are used to make viral proteins from the viral DNA found within the human DNA.
  6. The viral proteins are assembled into new viruses, which bud from the cell and go on to infect other cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Progression of AIDs?

A

Usual develops about 10 years after HIV infection.

  1. Initial symptoms of AIDS include minor infections of mucous membranes and recurring respiratory infections. These are caused by a lower than normal of T helper cells.
  2. As AIDS progresses number of T helper cells decreases further. Patients become susceptible to more serious infection including chronic diarrhoea, severe bacterial infections and TB.
  3. During late stages of AIDS, patients have a very low number of T helper cells and suffer from range of serious infections. These kill the patient, not AIDS itself.

Length of time someone survives depends on strain of HIV infected with, age, and access to healthcare.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe how some gets TB

A
  1. Mycobacteriun tuberculosis causes the disease TB.
  2. Infection occurs when tiny droplets containing the bacteria are inhaled into the lungs.
  3. In the lungs, the bacteria are taken up by a phagoctye.
  4. The bacteria survive and replicate inside the phagocyte.
  5. Most don’t develop TB straight away. Their immune system seals off infected phagocytes in structures in the lungs called tubercles.
  6. When sealed inside the tubercles the bacteria become dormant and person shows no symptoms.
  7. Later on, dormant bacteria reactivate and overcome the immune system, causing TB.
  8. Reactivation is more likely in people with weakened immune systems such as people with AIDS.
  9. Infection by mycobacterium tuberculosis and development of TB varies from weeks to years.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the progression of TB

A
  1. Initial symptoms of TB include fever, general weakness and severe coughing, caused by inflammation of the lungs.
  2. As TB progresses, it damages the lungs. If left untreated this can lead to respiratory failure and ultimately death.
  3. TB can also spread from lungs to other parts of body, eg brain and kidneys. This can cause organ failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 major entry routes of pathogens?

A
  1. Though cuts in the skin.
  2. Through the digestive system via contaminated food or drink.
  3. Through respiratory system by being inhaled.
  4. Through other mucosal surfaces e.g inside nose or mouth or the genitals.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Barriers to prevent infection?

A

Stomach acid- pathogens killed by acidic conditions. However some may survive and pass into intestines and cause disease.

Skin- acts a physical barrier to pathogens. If skin damaged blood clots at the area of damage to prevent pathogens from entering, but some may get in before it forms.

Gut and skin flora- intestines and skin naturally covered in billions of harmless microorganisms. They compete with pathogens for nutrients and space. The limits the number of pathogens living in the gut and on the skin.

Lysozyme- mucosal surface produce secretions. These secretions all contain an enzyme called lysozyme, which kills bacteria by causing lysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 mechanisms of the non-specific immune response?

A
  1. Inflammation at the site of infection:
    Immune system cells recognise foreign antigens and release molecules that trigger inflammation.
    These molecules cause vasodilation at site of infection increasing blood flow to it.
    This brings loads of immune system cells to site of infection which can then start to destroy the pathogen.
  2. Production of anti-viral proteins called interferons.
    When cells infected with viruses, they produce interferons, which prevent spread of virus to other cells by:
    A. Preventing viral replication by inhibiting production of viral proteins.
    B. Activate cells involved in specific immune response to kill infected cells.
    C. Activate other mechanisms of the non-specific response e.g. inflammation.
  3. Phagocytosis and lysozyme action.
    A. Phagocyte recognises antigens on a pathogen.
    B. Cytoplasm of phagocyte moves round the pathogen, engulfing it.
    C. Pathogen now in phagosome.
    D. Lysosome fuses with phagosome to form phagolysosome. Digestive enzymes break down pathogen.

E. Phagocyte then presents the pathogens antigens. It sticks the antigens on surface to become APC and activate other immune system cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe activation of T cells by phagocytes.

A
  1. T cell is a type of white blood cell. Surface covered in CD4 receptors.
  2. CD4 receptors on T cells bind to antigens displayed by APCs such as macrophages (type of phagocyte).
  3. Each T cell has diff shaped receptor specific to a complementary antigen.
  4. When T cell receptor binds to specific antigen it activates T cell causing it to divide.
  5. Different types of T cells carry out different functions:

T helper cells- release substances to activate B cells, T killer cells and macrophages.

T killer cells- attach to antigens on a pathogen-infected cell and kill the cell.

T memory cells

17
Q

Describe activation of B cells by T helper cells?

A

B cells are another type of white blood cell. Covered in proteins called antibodies.

Antibodies bind to antigens to form an antigen-antibody complex.

Each B cell has diff shaped antibody on its surface.

When the antibody on B cell meets complementary antigen so each B cells binds to diff antigen.

This together with cytokines released from the T cell, activates the B cell.

The activated B cell divides by mitosis into plasma cells and B memory cells.

18
Q

Antibody production?

A

Plasma cells are clones of the B cells
They secrete loads of the antibody, specific to the antigen, into the blood.
These antibodies will bind to the antigens on the surface of the pathogen to form lots of antigen-antibody complexes.

Antibodies are made of 4 polypeptide chains- 2 heavy chains and 2 light chains. Each chain has a variable region and a constant region.

The variable regions of the antibody form the antigen binding sites. The shape of the variable region is complementary to a particular antigen so differ between different antibodies.

Hinge region allows flexibility when the antibody binds to the antigen.

The constant regions allow binding to receptors on immune system cells e.g. phagocytes. Constant region sane in ALL antibodies.

Disulfide bridges hold the polypeptide chains together.

19
Q

How do antibodies clear infection?

A
  1. Agglutinating pathogens - each antibody had 2 binding sites, so an antibody can bind to 2 pathogens at the same time- the pathogens become clumped together. Phagocytes then bind to the antibodies and phagocytose a lot of pathogens all at once.
  2. Neutralising toxins- antibodies can bind to toxins produced by pathogens. This prevents the toxins from affecting human cells, so the toxins are neutralised. The toxin-antibody complexes are also phagocytosed.
  3. Preventing the pathogen binding to human cells- wjen antibodies bind to the antigens on pathogens, they may block the cell surface receptors that the pathogens need to bind to the host cells. This means the pathogen can’t attach to or infect the host cells.
20
Q

Membrane- bound and secreted antibodies?

A

Antibodies have two forms- they can be membrane-bound or can be secreted.

The two forms have slightly different heavy chain proteins.

Both heavy chain proteins are coded for by a single gene, which is copied into mRNA for protein synthesis.

It’s possible to create more than one proteins from the heavy chain gene by modifying the mRNA (splicing).

21
Q

Describe splicing.

A

Genes contain sections that don’t code for amino acids called introns.

Bits that do code for amino acids are called exons.

During transcription the introns and exons both copied into mRNA. This is called pre-mRNA.

The introns are then removed by splicing. Introns are removed and exons joined forming mRNA strands. Takes place in nucleus after transcription.

Sometimes certain exons are also removed as well as introns to form different mRNA strands. This is called alternative splicing.

This means that more than one amino acid sequence and so more than one protein can be produced from one gene.

22
Q

Describe how the production of memory cells gives immunity.

A
  1. When a pathogen enters the body for the first time the antigens on its surface activates the non-specific immune response. This then activates the specific immune response. Together these 2 make up the primary response.
  2. The primary response is slow because there aren’t many B cells that can make the antibody needed to bind to the antigen.
  3. Eventually the body will produce enough of the right antibody to overcome the infection, while the infected person will show symptoms.
  4. After exposure to an antigen, both T and B cells produce memory cells. These memory cells remain in the body for a long time. T memory cells remember the specific antigen and will recognise it a second time round. B memory cells record the specific antibodies needed to bind to antigen.
  5. The person is now immune- their immune system has the ability to respond quickly to a 2nd infection.
  6. If the same pathogen enters the body again, the immune system will produce a quicker, stronger immune response called the secondary response.
  7. T memory cells divide into the correct type of T cells to kill the cell carrying the antigen. B memory cells divide into plasma cells thay produce the right antibody to the antigen.
  8. The secondary response often get rid of pathogens before you show symptoms.
23
Q

Passive and active immunity?

A

Active immunity is when immune system makes its own antibodies after being stimulated by an antigen.
1. Natural active immunity is immunity you get after catching disease.
2. Artificial active immunity is the immunity you get after a vaccination.

Passive immunity is immunity you get from being given antibodies made by a different organism:
1. Natural Passive immunity is when a baby gets immunity from antibodies it receives from its mother, through the placenta and in breast milk.
2. Artifical Passive immunity is immunity after being injected with antibodies e.g. tetanus shot.

24
Q

How do vaccines give immunity?

A
  1. While your B cells are busy dividing to build up their numbers to deal with a pathogen you suffer from disease. Vaccination prevents this.
  2. Vaccines contain antigens that stimulate the primary immune response against a particular pathogen, without the pathogen causing disease. This means your body produces memory cells without ever having the disease as pathogens in vaccine are attenuated.
  3. Some vaccines contain many different antigens to protect against different strains of pathogens. Different strains of pathogens created by antigens variation.
25
Evasion mechanisms of HIV?
1. HIV kills the immune system cells that it infects. This reduces the overall number of immune system cells in the body, reducing chance of HIV being detected. 2. HIV has a high rate of mutation in the genes that code for antigen proteins. The mutations change the structure of the antigens and this forms new strains of the virus - this process is called antigenic variation. Memory cells produced for one strain of HIV won't recognise other strains with different antigens, so the immune system has to produce a primary response against each new strain. 3. HIV disrupts antigen presentation in infected cells. This prevents immune system cells from recognising and killing the infected cells.
26
Evasion mechanisms of mycobacterium tuberculosis?
When mycobacterium tuberculosis bacteria infect the lungs they're engulfed by phagocytes. Here, they produce substances that prevent the lysosome fusing with phagosome. This means the bacteria aren't broken down and they can multiply undetected in phagocytes. This bacterium also disrupts antigen presentation in infected cells, which prevents immune system cells from recognising and killing the infected phagocytes.
27
What the two types of antibiotics?
Bacteriocidal: kills bacteria. Bacteriostatic: prevent growth of bacteria.
28
What the two types of antibiotics?
Bacteriocidal: kills bacteria. Bacteriostatic: prevent growth of bacteria.
29
How do antibiotics work?
They kill or inhibit growth of barriers by interfering with metabolic reactions that are crucial for the cell. 1. Some inhibit enzymes needed to make the bonds in bacterial cell walls. This prevents the bacteria from growing properly. It can also cause cell death by causing lysis ad weakened cell wall cannot handle osmotic pressure. 2. Some inhibit protein production by binding to bacterial ribosomes. All enzymes are proteins, so if a cell can't make protein it can't make enzymes. This stops the bacteria form carrying out metabolic processes needed for growth and development.
30
Investigating the effects of antibiotics on bacterial growth?
1. Use sterile pipette to transfer the bacteria to an agar plate. Spread the bacteria over the plate using a sterile spreader. 2. Use sterile forceps to place paper discs soaked with different antibiotics spaced apart on the plate. Include negative control disc as well soaked in distilled water. 3. Lightly tape lid onto petri dish, invert and incubate for 48 hours at 25 degrees Celsius. Areas where bacteria unable to grow is called the door of inhibition. 4. Zone of inhibition can be measured using pi × r². Larger zone of inhibition = more effective antibiotic. Aseptic technique must be used throughout including: Regularly disinfecting surfaces Using sterile equipment Working near bunsen flame so any microbes in the air are drawn away from your culture.
31
How can hospital acquired infections be transmitted?
Hospital staff and visitors not washing their hands before and after visiting a patient. Coughs and sneezes not being contained. Equipment and surfaces not being disinfected.
32
What codes of practise have been developed to prevent and control HAIs?
Hospital staff and visitors should be encouraged to wash their hands, before and after they've been with a patient. Equipment and surfaces disinfected after use. People with HAIs should be moved to an isolation ward so they're less likely to transmit the infection to other patients.
33
What codes of practise have been put in place specifically to prevent HAIs caused by antibiotic-resistant bacteria?
Doctors shouldn't prescribed antibiotics for minor bacterial infections or viral infections. Doctors shouldn't prescribed antibiotics to prevent infections. Doctors should use narrow-spectrum antibiotics(which only affect specific bacterium) if possible Doctors should rotate use of different antibiotics. Patients should take all of antibiotics prescribed so infections are fully cleared.