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Biology > Topic 2 - C > Flashcards

Topic 2 - C Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is Mitosis?

A

The production of 2 genetically identical daughter cells by cell division

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2
Q

What is Mitosis used for?

A
  • growth and repair

- asexual reproduction

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3
Q

Explain what happens in the G1 phase?

A
  • normal cell activity and growth phase
  • mRNA and proteins prepare the cell for division
  • controlled by Cyclin and Cyclin-dependant Kinase which promotes DNA replication
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4
Q

What happens in G1 is DNA damage is detected?

A

Apoptosis - programmed cell death

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5
Q

Describe what is the restriction point in G1?

A

The cell is ready for division and moves to S phase.

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6
Q

Describe what happens in S phase?

A

DNA synthesis replicates the genetic material so each chromosome now consists of two sister chromatids

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7
Q

Describe what happens in G2 phase?

A
  • cells continue to grow and produce new proteins
  • another checkpoint to check if DNA is damaged, if so transition to mitosis is delayed
  • p53 protein is important in prevention of cancer
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8
Q

Describe the process of prophase?

A
  • nuclear membrane breaks down and nucleolus disintegrates
  • chromosome condense and now are visible
  • centrosome duplicate and move to opposite ends (poles) of cell and form spindle fibres
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9
Q

Describe the process of metaphase?

A
  • chromosomes line themselves in the middle of the cell

- attached to the spindle fibres by their centromere

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10
Q

Describe the process of anaphase?

A
  • centromere divides

- sister chromatids are pulled apart by spindle fibres and move to opposite ends of the cell

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11
Q

Describe the process of telophase?

A
  • nuclear membrane reforms around the chromosomes grouped at either poles of the cell
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12
Q

Describe the process of cytokinesis?

A
  • cytoplasm divides and there are now 2 genetically identical daughter cells
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13
Q

What causes cancer?

A
  • loss of cell cycle control

- uncontrollable cell division

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14
Q

Explain controlled cell division?

A
  • differentiation is when you are able to stop dividing

- programmed cell death - APOPTOSIS

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15
Q

Explain control mechanisms break down?

A
  • if enough nutrients are supplies then uncontrollable cell division, tumour (mass of cancer cells)
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16
Q

Which mutated protein can cause cancer?

A
  • p53 protein (which checks for damaged DNA in G2) is mutated and can’t control cell division
  • proto-oncogenes go into overdrive
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17
Q

What are oncogenes?

A
  • genes which stimulate cell division (growth factors and cell cycle regulation)
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18
Q

What are tumour suppressor genes?

A
  • genes that prevent tumour formation by repairing damaged DNA and regulating cell division to promote apoptosis
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19
Q

What are some causes of cancer?

environmental, genetic

A
  • mutations passed on from parents
  • somatic, happens after fertilisation
  • environmental factors (smoking)
  • viruses (HPV)
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20
Q

Briefly go over the cell cycle?

A

G1 - pre-replication gap - cell gets bigger

S - synthesis of DNA

G2 - pre-mitotic gap - cell replicates organelles

M - mitosis

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21
Q

Describe the process of binary fission?

A
  1. DNA replication
  2. Cell elongation
  3. Septum formation
  4. Cell separation - each daughter cell receives 1 chromosomes and a variable number of plasmid
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22
Q

Why don’t viruses undergo mitosis?

A

Viruses are non-living which means they inject nucleic acid into infected host cell and replicate

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23
Q

Explain what benign tumours are?

A
  • they are localised (one place) tumours which may compress onto functional tissue but don’t spread
  • they can be removed by surgery of destroyed by radiation
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24
Q

Explain what malignant tumours are?

A
  • they can travel in your body and cause other tumours, METASTASIS
  • more difficult to treat
  • chemotherapy and radiotherapy used to specifically target and kill rapidly dividing cells
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25
Q

Difference between benign and malignant tumours?

A

Benign Malignant
Slower growth rate Faster growth rate
Well-differentiated cells De-differentiated cells
Cell produce a capsule made Tumour not in capsule
of dense tissue No adhesion - metastasis
Cell produce adhesion molecules

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26
Q

What are the treatments for cancer?

A

There is no single treatment but most work by stopping DNA replication and mitosi.

Adriamycin + Cytoxan - stop DNA unwinding
Methotrexate - stop cells making DNA nucelotides
Taxol + Vincristine - inhibit spindle fibres

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27
Q

What are non-specific defence mechanisms?

A
  • physical barriers

- phagocytosis

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28
Q

What are specific defence mechanisms?

A
  • cell mediated T lymphocytes

- humoural response - B lymphocytes

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29
Q

Name some physical barriers?

A
  1. lysosomes - in tears/ secretion
  2. skin - fatty acids and flora
  3. cilia - removes particles in nasopharnyx
  4. mucus lining trachea
  5. rapid change of stomach - pH 2
  6. flushing of unrinary tract
30
Q

Describe what antigens are?

A

Foreign (non-self) macro-molecules

31
Q

Why do not all antigens provoke a immune response?

A

There are self antigens and harmless antigens like food, protein, pollen and dust - suppression of the immune system to harmless macro-molecules ion highly regulated to prevent damaging process to host - tolerance.

32
Q

What are epitopes?

A
  • small components of antigens recognised by receptors on T and B cells
33
Q

Describe the entire process of phagocytosis?

A
  1. Pathogens or damaged cells produce chemoattractants
  2. Phagocytes move towards chemoattractants
  3. Phagocytes bind to pathogen
  4. Phagocytes engulf pathogen in vesicle called phagosomes
  5. Lysosomes fuse with phagosomes and release hydrolitic enzymes
  6. Pathogen is digested to form small molecules - some used by cell
  7. Antigens are now attached to cell membrane - phagocyte not an Antigen Presenting Cell (APC)
34
Q

What are examples of APC’s

A
  1. Dendritic cells - immune cells in skin, lining of nose, lungs, intestines
  2. Macrophages - B cells before activation and differentiation
  3. Tumour cells - unusual antigens on the surface
  4. Infected cells - viral membrane of protein
35
Q

Why do lymphocytes take days/weeks to be established?

A

Once a lymphocyte has been activated it takes a few days for clonal expansion to be completed then lymphocytes must differentiate into effector cells.

36
Q

Where do T lymphocytes mature?

A

Bone Marrow

37
Q

Where do B lymphocytes mature?

A

Thymus

38
Q

Describe the role of a Helper T cell?

CD4

A
  • activate B cells and cytotoxic cells by secreting cytotokines
  • responds to APC’s
39
Q

Describe the role of a Cytotoxic cell?

CD8

A
  • destroy virus infected cells

- emit cytokines to amplify immune response

40
Q

How are lymphocytes activated?

A
  • activated when they bind with antigens presented on APC
41
Q

Explain what the receptors on T cells do and their function?

A

CD4 and CD8 receptors regulate how T cells interact and respond to APC

42
Q

Describe the entire process of activation and action of cytotoxic cells?

A
  1. APC displays antigens from pathogen in cell membrane
  2. Cytotoxic cells with complementary receptors bind to antigen
  3. Cytotoxic cells divide rapidly by mitosis to form clones
  4. Some of cloned cells develop into memory cells
  5. The cloned killer cytotoxic cells phagocytes to engulf pathogen
43
Q

How do cytotoxic cell actually kill infected cells?

A

They produce a protein (preferin) that makes holes in infected body’s cell membrane and secrete toxins and enzymes killing the cell

44
Q

Describe the entire process of B lymphocytes activation and action?

A
  1. B cells receptors bind to specific antigen
  2. B cells present antigens to T helper cells so they can activate them
  3. B cells are now activated to divide by mitosis and form clones of B cells
  4. Each mature into a plasma or memory cell
  5. Plasma cells secrete antibodies
45
Q

Why are antibodies soluble?

A

They need to diffuse through blood stream.

46
Q

Describe how antigen-antibody complex forms?

A
  • antigen binding site is specific and complementary to one particular antigen which fits it perfectly
  • the area is a specific 3D shape and differs due to variable region
47
Q

Explain agglutination?

A

Agglutins clump foreign substances together from preventing them from entering cells or reproducing.

48
Q

Why don’t we feel symptoms if we are re-infected?

A
  • immune response is faster

- as antibodies are being produces as a higher concentration

49
Q

What is the definition of a vaccine?

A

A vaccine contains antigens that produce memory against a particular pathogen without causing a disease.

50
Q

What is the definition of herd immunity?

A

The use of a vaccine to provide protection for individuals and population against the disease.

51
Q

Describe Active Immunity?

A

When an immune system makes its own antibodies after being stimulated by an antigen.

52
Q

Explain Active Natural Immunity?

A

Becoming immune after getting the disease.

53
Q

Explain Active Artificial Immunity?

A

Becoming immune after being vaccinated with harmless dose of antigen.

54
Q

Describe Passive Immunity?

A

Being given antibodies made be a different organism.

55
Q

Explain Passive Natural Immunity?

A

Being given antibodies from the mother through the placenta or breast milk.

56
Q

Explain Passive Artificial Immunity?

A

Being injected with antibodies.

57
Q

Why do we feel no symptoms during secondary infection?

A
  • quicker/faster immune response

- antibodies produced at a higher conc.

58
Q

State what a HIV virus contains?

A
  • RNA genetic material
  • attachment protein GP120 complementary to CD4 receptors
  • capsid
  • lipid envelope
  • matrix
  • reverse transcriptase enzymes
59
Q

Explain the HIV replication process?

A
  1. Attachment protein, GP120, attaches to a receptor, CD4, on the cell membrane of the host helper T-cell
  2. The capsid is released into the cell where it releases genetic material (RNA) into cell cytoplasm
  3. Inside the cell, reverse transcriptase enzymes is used to make complementary strand of DNA from 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 viral DNA
  6. The viral proteins are assembled into new viruses which bud onto the cell and infect new cells
60
Q

Why does HIV make the immune system susceptible?

A

They infect and eventually kill T helper cells which send chemical signals to phagocytes, cytotoxic T cells and B cells which are important in the immune response.

61
Q

How does HIV develop into AIDS?

A

As HIV replicates the number or T helper cells drops and when they drop below a certain level - it becomes AIDS.

62
Q

Why is AIDS so dangerous?

A

People with AIDS generally develop diseases that wouldn’t cause problems in an healthy immune system

63
Q

Describe the initial symptoms of AIDS?

A
  • minor infection of mucous membrane (inside nose, ear and genitals) and recurring respiratory infections
  • more susceptible to more serious infections like diarrhoea, severe bacterial infections and tuberculosis
  • toxoplasmosis of the brain (parasite infection)
  • candidiasis of respiratory system (fungal infection)

Both toxoplasmosis and candidiasis kill the patient not the HIV itself.

64
Q

Why are antibiotics ineffective to viruses?

A
  • antibiotics are designed to target and kill bacteria by interfering with their metabolic reactions such as bacterial enzymes and ribosomes, SO THEY DON’T DAMAGE HUMAN CELLS!
  • viruses don’t have their own ribosomes and enzymes as they inhibit a human cells
65
Q

State the uses of monoclonal antibodies?

A
  • diagnosis of disease (ELISA test for HIV)
  • treatment (therapy against cancer)]
  • passive immunity (antibodies given to treat septic shock)
  • detection and purification of biomolecules (used to look for specific protein e.g. pregnancy test)
66
Q

How do anti-cancer drugs work?

A
  1. Cancer cells have specific antigens called tumour markers
  2. Monoclonal antibodies can be made to bind to the tumour marker
  3. You can attach anti-cancer drug to antibodies so they’ll bind to tumour markers
  4. they only target cancer cells due to specificity meaning there will be lower side effects
67
Q

Explain how pregnancy tests work with monoclonal antibodies?

A
  1. Application area contains antibodies (that are complementary to hCG protein) bound to blue beads
  2. When urine is applied to the application area any hCG will bind to the antibody on the bead creating antigen-antibody complex
  3. Urine moves up the stick to the test strip, carrying any beads with it
  4. Test shape contains antibodies to hCG which are immobilised
  5. If hCG is present, the test strip turns blue as immobilised antibodies bound to hCG
68
Q

What is ELISA?

A

Enzyme linked immunosorbent assay

- which uses antibodies to detect a specific molecule

69
Q

What are the benefits of ELISA?

A
  • extremely sensitive, it will detect small concentrations creating a colour gradient
  • highly specific
70
Q

Explain the process of Direct ELISA?

A
  1. An antibody which is complementary to the antigen is added to your sample
  2. This antibody has an enzyme attached to it
  3. The wells are rinsed thoroughly to remove any unbound antibodies
  4. A substrate complementary to the enzyme is added
  5. If antibodies bind (due to antigen presence) and enzyme-substrate complex is formed which produces a colour change
71
Q

Explain the process of Indirect ELISA?

A
  1. Antigens are bound to inside the well plate
  2. A sample which may contain antibodies complementary to the antigen is added (primary antibody)
  3. Well is rinsed - to remove anything that hasn’t been bound so there isn’t a false result or colour change
  4. Enzyme linked to secondary antibodies are added which can bind to primary antibodies
  5. Wells are rinsed again - if no primary antibodies bound, the secondary antibodies would be washed away too
  6. A solution containing a substrate complementary to the enzyme is added - if enzyme-substrate complex is formed a colour change will occur
72
Q

What is a Chi-squared test used for?

A

Used to see whether observed frequency fits the frequency you expected.

Biology (5 decks)

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