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Biology U4 > 6B > Flashcards

6B Flashcards

1
Q

What is non specific response

A

Same regardless of the pathogen that invades the body

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2
Q

What’s is specific

A

Specific to particular pathogen

Able to recognise specific pathogen due to the presence of antigens on their cell surface

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3
Q

What steps of inflammation
Non specific

A

Mast cells respond to tissue damage by secreting histamine

This causes blood vessel to dilate leading to redness reducing the reproduction rate of pathogen

Histamine makes the cell forming the walls of the capillaries separate slightly thus making the Capillary walls become more permeable allowing fluids to enter the tissue and create swelling
—> releasing plasma contains leukocytes out forcing antibodies out of the capillaries
Disabling pathogens

The antibodies disable the pathogens and macrophages and neutrophils destroy them by phagocytosis

Phagocytes leave the blood and enter the tissue to engulf foreign particles

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4
Q

What do interons do

A

They inhibit the production of viral proteins preventing the virus from replication

They activate white blood cells involved with the specific immune response to destroy infected cells

They in case the non specific immune respe

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5
Q

How does fevers

Why does the Hypothalamus reset the body temperature higher
Non specific

A

Many pathogens reproduce quickly at 37c can’t below so higher temperatures will reduce their ability to effectively reproduce

Specific immune response function better at higher temperature making combat against the infection more successful

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6
Q

How is fever beneficial

A

Patient will start to sweat to cool the body down releasing fluid and electrolyte

If not replaced this could lead to severe dehydration it can cause enzyme to denature resulting permanent tissue damage

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7
Q

Phagocytosis

A

1)Chemicals released by pathogens as well as chemicals released by the body cells under attack

2)They move towards pathogen and recognise the antigens on the surface of the pathogen as Beng non-self

3) the cell surface membrane of phagocytes extend out and around the pathogen, engulfing it and trapping the pathogen within a phagocytes vacuole
—> endocytosis

4) enzyme are released into the phagocytic vacuole when lysosome fuse with it

5) these digestive enzyme, which includes lysosomes digest the pathogens

6)after digesting the pathogen , the phagocytes will present the antigens of the pathogen on its cell surface membrane

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8
Q

Where is T cell produced from

A

Produced in the bone marrow and activated in the thymus gland

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9
Q

What’s is T killer cell used for

A

Produce chemicals to destroy infected cells

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10
Q

What is helper T cell usedfor

A

Activate plasma cell to produce “ antigens - specific” antibodies and secrete opsonin to label pathogens for phagocytosis

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11
Q

T memory cell

A
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12
Q

Where is B cell produced and what it produces

A

Produced in the bone marrow

These cells have globular receptor proteins sued in producing immunoglobulin (antibodies

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13
Q

What does B effector cells do

A

Divide to form plasma clones

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14
Q

What does plasma cell

A

Produce antigen specific antibodies

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15
Q

B memory cell

A

Provide immunological memory (secondary response)

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16
Q

What does humoral response

A

Production of antibodies

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17
Q

Humoral response

A

T helper activation stage

Effector stage

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18
Q

T helper activation stage

A

1)Bacterium with antigens on surface

2) bacterium engulfed by a macrophages

3)macrophages present the antigens from the bacterium on major his to compatibility complexes (MHCs) it becomes an antigen presenting cell (APC)

4) a macrophages APC binds to T helper cell. Once the T cell is activated, it divides to form T memory cells and active T helper cell

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19
Q

Effector stage

A

1)Bacterium with antigens on surface

2) antigens binds to B a cell with complementary receptor. The B cell engulfs the bacterium by endocytosis and enzyme break it down to leave antigen fragments

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20
Q

Effector step 3

A

B cells becomes an APC

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21
Q

Effector step 4

A

An activated T helper cell with a complementary receptor binds to the APC. It produces cytokines that stimuli the B cell

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22
Q

Effector stage 5

A

The B cell divides to give B memory and B effector cells

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23
Q

Effector stage 6

A

B effector cells differentiate into plasma cell

Plasma cells secrete antibodies these bind to the antigens on other similar pathogens identifying them so they are easier to destroy

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24
Q

What is agglutination

A

Binding to antigens on pathogens to make them stick together

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25
Q

What is opsonisation

A

Antibodies act as an opsonin making pathogens more easily recognised by phagocytosis

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26
Q

What neutralisation

A

Binding to bacterial toxins to reduce their effect

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27
Q

Cell mediated response step 1

A

A bacterium infects a host cell

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28
Q

Cell mediated response step 2

A

Host cell present the antigens on MHCs and become an APC

29
Q

Cell mediated response step 3

A

T killer cell with complementary receptor binds to the APC

Cytokines from activated T helper cells

30
Q

Cell mediated response step 5

A

Stimulated by cytokines from the T helper cell the T killer cell divides and differentiate to form two clones one of the active T killer cells and one of T killer memory cells

31
Q

Cell mediated response step 6

A

The active T killer cells bind to infected cells presenting antigens on MHCs

32
Q

Cell mediated response step 7

A

The T killer cells releases chemicals causes lysis in the infected cell as pores form in the membrane the infected cell dies

33
Q

What happens in primary response

A

Number of T and B cells with correct membrane receptors are Low

To be activated and divide and differential into different cell types

It can take several days before plasma cells develops and are able to start producing antibodies against antigen
—> infected person will experience symptoms

Both B and T cells produce memory cells during the primary respe which will remain in the blood after infection is over

34
Q

Secondary response

A

Faster and stronger than the primary response

Memory cells are present in larger quantities tha the mature lymphocytes at the start of the primary response so the correct memory cell are able to detect an antigen activate divide by mitosis and differentiate much more quickly

Antibodies are produced more quickly and are in larger quantities

35
Q

Natural active immunity

A

When your body comes into contact with a foreign antigen, causing the immune system to be activated to produce antibodies against the pathogen to destroy it

36
Q

What is natural passive immunity

A

Temporary immunity given from the mother to the fetus , through the transfer of pro formed antibodies through placenta or the mother milk and this last until the fetus immune system become active

37
Q

Artificial passive immunity

A

Where antibodies from one individual are extracted and injected in another , which prevents development of the disease , but not give long term immunity

38
Q

Artificial active immunity

A

Small amount of a safe form the pathogen are used to grant immunity
- injection of detoxified form of toxin
-inactivated viruses or dead bacteria
-attenuated pathogens
-using fragments of outer coat of viruses

39
Q

Eradication of disease

A

Disease not found in either people animals or anywhere in the environment

40
Q

Elimination of disease

A

Disease disappears but remains in animals, the environment or mild infection so immunisation must continue regardless of the number of cases

41
Q

Here immunity

A

Large portion of the population is vaccinated against a disease, so that it becomes very difficult for the disease to keep affecting who can be vaccinated is vaccinated, so that those who cannot be vaccinated don’t catch the disease. It is important to provide herd immunity when there is a serious outbreak of a disease

42
Q

Drugs against micro-organism

A

Antibiotics destroy microorganisms or prevent them from reproducing, and along with immunisation this has cured many diseases.

Antibiotics work based on selective toxicity, by interfering with the chemistry or metabolism of the bacteria without affecting the human host

43
Q

What is bacteriostatic

A

Inhibit the growth of bacteria

44
Q

Define Bactericidal

A

Kills bacteria

45
Q

What are the 2 actions of bacteriostatic

A

Interrupting metabolic pathways to block nucleic acid or viral nutrients synthesis

Protein synthesis inhibition or prevention of transcription and translation of microbial genes

46
Q

What are Bactericidal 3 actions

A

1) prevent formation of cross linking cell walls to kill bacteria by lysis

2) damage the cell membrane so water moves in to metabolite or move out killing the bacteria

3) stop bacterial DNA winding into rings so that it can no longer fit inside the cell

47
Q

Factors that affect the antibiotics

A
  • concentration of drug around infected area
    -local pH
    -whether the pathogen or host cell destroy the antibiotics
    -susceptibility of pathogens to the antibiotics used
48
Q

Dose of drug

A

If the standard dose of drug destroy the pathogens and cures the disease, the pathogen is said to be sensitive to the antibiotic.

49
Q

Drug resistant

A

1) a group of bacteria include genetically resistant ones, are exposed to an antibiotic

2) most of the sensitive bacteria die

3) the genetically resistant bacteria starts multiplying

4) eventually the resistant strain replaces the strain affected by the antibiotics

50
Q

How to reduce selection pressure

A
  • use antibiotics only when strictly necessary
    -making sure people complete their antibiotics course
    -using as few different antibiotics as possible and introduce new antibiotics when possible
51
Q

MRSA

A

S.aureus can be the skin or inside nasal passage without affecting, once inside the body it can have negative effect

Treated with methicillin but has now develop3d a resistance

High dosage with narrow of drugs

52
Q

Clastrrdium difficile

A

This is an anaerobic bacteria which can be present in the body and not cause harm as they’re their number are limited

53
Q

Controlling the use of antibiotics

A

Antibiotics should be used carefully only when necessary
—> full course should be completed

If not completed the immune system will not be able to destroy all the bacteria, and so they can infect other people and grow resistant

54
Q

Hand washing

A

Wash their hands with alcohol based gels and chlorine disinfectant to destroy any pathogens. In addition they should wear appropriate clothing to avoid spreading pathogens

55
Q

Isolation of patients

A

HAI infected patients need to be isolated in high level of hygiene and disinfect rooms as to prevent the spread of infection

56
Q

Prevention of infection coming into the hospital

A

Patients carrying communicable disease need to be treated of them first before they are treated of the main infection

As to not spread infection. Moreover unwell people should not visit patients and when visiting visitors should maintain a high level of hygiene

57
Q

Monitoring levels of HAI

A

Measuring and reporting is important as it is attracts attention so that more effort are put to solve the problem

58
Q

Explain how a mutation in the genome could lead to the host suffering from influenza more than once

A

On the first infection the host immune system makes antibodies and memory cells against the virus antigens

If the same antigens are detected a secondary response is rapid and prevents symptoms developing

A mutation will alter the shape of the antigens

The host memory cells will no longer recognise the antigens

59
Q

Suggest why this might lead to secondary infection by bacteria

A

Ciliated cells move mucus up the respiratory tract

Infected cells die and the mucus stops moving

Bacteria are caught in the mucus
Ence ideal conditions and reproduce quickly
Bacteria experi

60
Q

Decomposition in nature

A
61
Q

Conditions for recycling nutrients

A

Warm and moist
—> higher temperature —> greater enzyme activity
—> not too high it going to denature

Moist
- makes dissolving easier
-prevent microorganisms from completely drying

Plenty of oxygen
-decays faster as decomposed respire faster

62
Q

Factors that affect the time of death fat level

A

Body fat slows down cooling because it acts as an insulator, and so a fatter person will cool slower than the thinner one

63
Q

Factors that affect the time of death mode of death

A

Someone who died in a cold area will cool faster than in a warm area

64
Q

Factors that affect the time of death surrounding temperature

A

Someone who died in a cold area will cool faster than in a warm area

65
Q

Factors that affect the time of death surface area ; volume

A

Smaller people cool faster as diffusion is more sufficient

66
Q

Factors that affect the time of death clothing

A

Clothes and covering insulate the body and so it cools slower

67
Q

Rigor mortis

A
68
Q

What are vaccine

A

Contains antigens whichare put into the body for active artificial

Vaccines contain dead or weaken pathogen less harmful strain

69
Q

How vaccination work

A

Vaccination produce long term immunity as they cause memory cell to be created

The immune system recognise the antigens when re-encountered and produce antibodies in a faster, stronger secant response

Biology U4 (9 decks)

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