Topic 6 Wood Flashcards
1
Q
Structures only in Prokaryotes
A
cell wall slime capsule flagellum pilli DNA loop
2
Q
Structures only in Eukaryotes
A
Golgi sER rER centrioles lysosomes nucleus, nucleolus, nuclear pore mitochondria
3
Q
Structures in both Prokaryotes and Eukaryotes
A
cytoplasm
ribosomes (although different sizes)
cell membrane (pro - cytoplasmic, eu - plasma)
4
Q
Features of Prokaryotes
A
- smaller
- always unicellular
- no nucleus
- no membrane bound organelles
- DNA is circular without proteins
- ribosomes are small (70S)
- no cytoskeleton
- motility by rigid rotating flagellum
- cell division by binary fission
- reproduction is asexual
5
Q
Features of Eukaryotes
A
- larger cells
- often multicellular
- always have nucleus
- have membrane bound organelles
- DNA is linear and associated with proteins forming chromatin
- ribosomes are larger (80S)
- always has cytoskeleton
- motility by flexible waving cilia or flagellae
- cell division by mitosis or meiosis
- reproduction asexual or sexual
6
Q
What is the basic structure of a virus?
A
a protein coat and nucleic acid (can be DNA or RNA)
7
Q
Viruses can come in wide shapes and sizes but…
A
…always based around protein coat and nucleic acid
8
Q
Gram positive bacteria
A
has relatively large amounts of peptidoglycan and no lipopolysaccharides
- uptakes crystal violet
- doesn’t uptake safranin
- goes purple/ violet after staining
9
Q
Gram negative bacteria
A
small amounts of both peptidoglycan and lipopolysaccharides
- doesn’t uptake crystal violet
- uptakes safranin
- goes pink after staining
10
Q
What are the 2 types of immune response?
A
non-specific - has an immediate effect
specific - delayed effect
11
Q
What are the 2 types of non-specific immune response?
A
Active defence - deals with microbes once they’re in the body
Passive defence - prevents entry of microbes
12
Q
Pathogens can’t cause disease due to barriers:
A
non-specific (physical and chemical) and cellular defences that prevent them from entering the body
13
Q
Antigens analogy
A
antigens are little flags on every cell type. All the cells in your body have one colour flag and everything else will be different colour flags so when your body sees a different colour flag it reacts
14
Q
Physical barriers
A
prevent entry of pathogens and microbes when intact
15
Q
Skin
A
- huge barrier (biggest organ)
- secretes sebum which lowers the pH –> inhibits pathogen growth
- sweat contains salt and enzymes making it hard for bacteria to live there
- blood clotting prevents entry of microbes through wounds
16
Q
Sebum
A
natural oil skin produces (always) that keeps skin soft and allows elasticity and flexibility of skin (collagen fibres help)
17
Q
Tears
A
contains lysozymes which are enzymes that can destroy bacterial cells (by breaking down their cell walls) preventing entry of pathogens in the eye
18
Q
Eyelashes
A
responds to foreign bodies near the eyes = blinking = causes eddy currents by the eye
19
Q
Respiratory tract
A
mucus and ciliated cells = goblet cell produces mucus, wafts to swallow or cough up mucus
20
Q
Digestive system
A
stomach acid which lowers the pH (1.5-2.5) = inhospitable environment for bacteria to survive
21
Q
When barriers fail…
A
microbes can enter the bloodstream and cause an infection
22
Q
You get inflammation from:
A
- a burn
- excess sun
- a scratch
- damage from a cut
23
Q
Inflammation
A
- blood clot to seal injury
- WBCs and mast cells in connective tissue below the skin surface release HISTAMINES (why you get antihistamines)
- area feels warm and becomes swollen
24
Q
HISTAMINES cause…
A
- arteriole dilation therefore increasing blood flow
- increase permeability of capillary wall (becomes leaky). This means plasma, WBCs and antibodies move into the tissue fluid (oedema). Fibrinogen also moves in and seals off the area preventing blood poisoning
25
Interferon
- is a natural antiviral agent which interferes with viral infection
- virus infected cells produce this protein
- interferon diffuses to surrounding tissues and inhibits viral replication by interfering with protein synthesis
26
Phagosome
vesicle surrounding the pathogen
27
Phagolysosome
point at which phagosome and lysosome fuse together
28
the 3 main types of WBCs are:
- neutrophils (phagocytic)
- monocytes (phagocytic)
- lymphocytes
29
Phagocytosis
process in which invading microbes are engulfed and destroyed by specific white blood cells known as phagocytes
30
Phagocytosis steps
- pathogen attached to phagocyte by antigen and surface receptors
- pathogen engulfed by infolding of phagocytic membrane
- lysosomes swarm to phagosome and release lysins into phagosome
- harmless end products of digestion are absorbed
31
What do phagocytes (especially neutrophils) produce? Why?
Highly reactive radicals (nitric oxide and superoxide). This kills engulfed bacteria by attacking their DNA and proteins
32
What are the 2 functions of a macrophage?
phagocytosis and antigen presentation
33
What are the 2 main types of specific immune response?
- cellular/ cell mediated response involves highly specialised cells to target pathogens inside cells
- humoral or antibody mediated response targets pathogens in body fluids with antibodies
34
How are lymphocytes activated?
Lymphocytes can only be activated by one particular antigen
35
Where do mature lymphocytes circulate?
in the spleen, lymph nodes, adenoids and tonsils as well as the lymphatic system and general circulation of the body
36
Where do lymphocytes originate from?
stem cells in the bone marrow
37
B lymphocytes
mature in the bone marrow, then migrate to the lymph nodes, they produce antibodies
38
T lymphocytes
migrate to the thymus gland for a period of maturation before migrating to the lymph nodes
39
Cellular immune response (step 1)
When a macrophage destroys a pathogen by phagocytosis, it displays the pathogen's antigen on its surface. It's now an APC (antigen presenting cell). Waste products are expelled but antigen is kept and presented on the MHC (major histocompatibility complex)
40
Cellular immune response (step 2)
APC releases first cytokine; a chemical involved in cell signaling. APC interacts with T helper cell, then releases (bind to CD4 receptor on T helper cell)
41
Cellular immune response (step 3)
First cytokine stimulates the T helper cell into releasing another cytokine. This second cytokine stimulates the growth and development of antigen specific T killer cells
42
Cellular immune response (step 4)
T killer cells identify the antigen on the surface of infected body cells and produce perforin. This protein forms pores in the target cell membrane allowing ions and water in causing lysis of the cell.
43
Cellular immune response (step 5)
T memory cells formed as a result of 'explosion'. These like to hover round the spleen
44
Humoral immune response (step 1)
When a macrophage destroys a pathogen by phagocytosis it will display the pathogen's antigen on its surface. The cell is now an APC where the antigen is presented on the MHC
45
Humoral immune response (step 2)
The APC interacts with a T helper cell - binds to CD4 receptor and releases a cytokine
46
Humoral immune response (step 3)
The first cytokine stimulates the T helper cell to release another cytokine which stimulates the differentiation of effector B cells into plasma cells
47
Humoral immune response (step 4)
The plasma cells divide by mitosis and produce large quantities of antigen specific antibodies. These can attach to the pathogen and destroy it by neutralisation, agglutination, opsonisation
48
Opsonisation
mark cells for destruction
49
Agglutination
clumps and sticks cells together
50
Neutralisation
specific antibodies block sites on virus' that they use to enter target cells
51
Humoral immune response (step 5)
Exposure to specific antigens also results in memory B cells being produced. These are ready to initiate a response to the same pathogen if the body becomes infected again in the future
52
How does the second infection by the same pathogens' response differ from the first?
- the immune response is much larger
- pathogens are killed much quicker
- the host recovers from the infection without suffering from any symptoms
53
Second infection by the same pathogen
- Macrophages migrate into the tissue fluid around the infected cells
- They engulf and digest the pathogens
- The become APCs: memory T cells undergo clonal expansion, foreign antigens on the APCs attach to receptors on the specific memory T cells, helper T cells and killer T cells are formed, helper T cells and APCs attach to receptors on the specific memory B cells, the memory B cells become plasma cells, plasma cells secrete antibodies
54
HIV
Human Immunodeficiency Virus
55
AIDs
Acquired Immunodeficiency Syndrome
56
How is HIV passed on?
via bodily fluids: blood, semen, vaginal, rectal secretions, breast milk
57
HIV treatments
- reverse transcriptase inhibitors: prevent viral RNA being copied into DNA for protein synthesis
- protease inhibitors: inhibit proteases used for synthesis of viral proteins
58
Why are HIV treatments not effective?
they only suppress the virus not kill them as you'd have to kill your own cells and you.
59
What type of drugs are reverse transcriptase and protease inhibitors?
antiretroviral drugs designed to target different stages in its life cycle. HIV can develop resistance to these drugs so patients often take a combination
60
Acute phase of HIV
- HIV antibodies appear in the blood
- symptoms; fever, sweats, headaches, sore throat, swollen lymph nodes or no symptoms
- loss of T helper cells
- T killers recognise infected T helper and destroy them
61
Latent/ Chronic phase of HIV
- symptoms: longer to recover from mild illnesses, possibly no symptoms
- dormant disease may reactivate (TB, shingles)
62
Disease phase of HIV
- increase viral load and decreased T helper cells results in AIDs
- opportunistic infections are likely to be fatal
63
Immune
if you come into contact with the pathogen in the future , you can rapidly destroy the pathogen before the onset of any symptoms
64
Vaccine
dead or weakened versions of a pathogen injected into your body for you to fight off as normal but without the effects
65
Active immunity
your immune system makes its own antibodies after being stimulated by antigens that have entered the body
66
Passive immunity
antibodies are made by another organism (aren't made by you)
67
Herd vaccination
vaccinate most/all people - stops infection spreading within population
68
Ring vaccination
vaccinate all people around victim - contains spread within ring, stops transmission (trace/ isolate contacts, travel restrictions)
69
Pros of vaccination
- can save lives
- protect vulnerable people in population
- controlled dosage
- protect the 'herd'
- save time/ money on medicine
- protect future generations
70
Cons of vaccination
- side effects
| - contain harmful ingredients
71
Passive natural
antibodies pass from mother to baby via milk or placenta - protects baby for a short time
72
Active natural
body makes own antibodies in response to antigen - develops following infection
73
Passive artificial
person is given ready made antibodies - immediate protection in emergency cases but short lived - broken down after days/ weeks
74
Active artificial
develops following immunisation - antigens in vaccine trigger specific immune response
75
Vaccines can contain:
Attenuated viruses - weakened viruses which are harmless
Killed bacteria
Toxin altered into harmless form
Antigen bearing fragment of the pathogen
76
Booster vaccines...
...ensure long lasting immunity
