Module 4 Flashcards
1
Q
Malaria
A
- caused by proctoctists - plasmodium vivax
- carried by vector- female anopheles mosquito
- also transmitted by blood transfusions and across the placenta
2
Q
Life cycle of malaria
A
- person with malaria has gametes of P.vivax in blood
- person bitten by female anopheles mosquito and gametes in blood go to its stomach
- gametes fuse and zygotes of P.vivax develop in its stomach
- develop into infective stages and migrate to salivary glands
- mosquito bites uninfected person and injects saliva containing infective P.vivax
- infective stages enter hosts liver and divide by mitosis
- these enter the blood to feed on haemoglobin in red blood cells and make more gametes
3
Q
HIV
A
- HIV causes AIDS
- HIV +VE = inactive version of virus present so no symptoms of aids, can go unknown for a long time ( in which it may be transmitted)
- active version destroys t helper cells
- lowers ability to destroy pathogens
- increased likelihood of contracting aids related diseases ( e.g pneumonia )
4
Q
Why HIV/AIDS higher in sub-Saharan africa
A
- poverty
- less education about means of transmission
- more promiscuity/ people working in the sex industry
- lower condom availability
- religious reasons for not wearing condoms
- countries promoted denial of existence
- fewer medicinal facilities for screening
- less screening of blood for transfusions
- more infected mothers have to breast feed- no alternative
- more cases of rape
- more intravenous drug abuse
- more use of shared needles
5
Q
Tuberculosis
A
- caused by bacteria: Mycobacterium tuberculosis and M. bovis
- transmitted by droplet infection ( coughs and sneezes )
- usually in lungs
- also transmitted through milk or meat of infected cattle
6
Q
what conditions make tuberculosis more likely?
A
- overcrowded living conditions
- poor ventilation
- weakened immune system
- poor diet
- homelessness
- living or working with people who have just migrated from areas with high TB prevalence
7
Q
why hasn’t TB been eradicated
A
- LEDCs cant afford vaccines/ antibiotics
- vaccine not 100% effective
- bacteria have become antibiotic resistant
- people don’t finish long antibiotics course
- lack of education
- people drink unpasteurised milk (LEDCs)
- migration of carriers with no symptoms
8
Q
Phagocytosis
A
- phagocytes engulf and digest pathogens
- receptors on phagocyte cell surface membrane bind to antigen on pathogen cell surface membrane
- produces a phagosome
- lysosymes fuse with phagosome releasing lysins into it
- pathogen is digested into amino acids, fatty acids etc
- products absorbed into cytoplasm by diffusion
9
Q
structure and function of antibodies
A
- 4 polypeptide chains held together by disulphide bonds. Y shaped molecule
- constant region to bind to phagocytes
- variable region complementary in shape to antigen to bind to pathogen
- more than one variable region allows attachment to more than one antigen and more than one pathogen for agglutination
- hinge region allows flexibility of branches of Y shaped molecule to move closer or further to bind to multiple antigens
- causes neutralisation by blocking binding sites
- light and heavy chains
10
Q
role of antibodies
A
- bind to antigens on pathogens cell surface membranes
- neutralises pathogens
- antibodies cover binding sites on pathogen
- prevents entry to host cell
- agglutination of pathogens
- multiple variable regions allow antibody to clump pathogens together
- clump too large to enter host cell and increases likelihood of being consumed by phagocyte
- antitoxins neutralise toxins
- opsonins allow phagocytes to bind to them ( binded to pathogen ) to perform phagocytosis
11
Q
immune response: T lymphocytes - cellular response
A
- macrophages engulf and digest pathogens, incorporate pathogens antigens into their cell surface membrane- antigen presenting cells
- helps select specific t lymphocytes with receptors complementary in shape to antigen ( clonal selection )
- once correct are selected, divide by mitosis in clonal expansion
- t helper cells release cytokines which are specific shapes and bind to complementary receptors on B lymphocytes stimulating them to divide by mitosis and differentiate. also stimulate macrophages to carry out more phagocytosis
- t killer kill infected host cells by secreting protease enzyme into them
- t memory cells stay in blood in case secondary infection by the same pathogen. allow a faster secondary response as they recognise the antigen and make clones and differentiate to form new t cells more quickly than in primary response
12
Q
Immune response - B lymphocytes ( humoral response )
A
- specific B lymphocytes with receptors complimentary in shape to the antigen or invading pathogen are selected- clonal selection
- cytokines released by t helper hells stimulate B lymphocytes to divide by mitosis in clonal expansion and then to differentiate into plasma cells and B memory cells
- plasma cells produce and secrete antibodies which are complimentary in shape to the antigen, these cause agglutination or neutralisation of the pathogens.
- B memory cells stay in the blood in case there is a secondary infection by the same pathogen. They allow a faster secondary response because they recognise the antigen and can make clones and change to form new antibodies so new antibodies are made more quickly than in the primary response.
13
Q
Examples of cell signalling in the immune response
A
- pathogens antigens communicate to the body that they are foreign
- infected cells with foreign antigens on surface communicate to lymphocytes to be selected in clonal selection and to T killer cells that they need to be killed
- macrophages engulf and incorporate pathogens antigens on their cell surface membrane communicate to t lymphocytes to be selected in clonal selection
- t helper cells release cytokines ( interleukins ) which bind to receptors on B cells and stimulate them to divide by mitosis and differentiate
- macrophages also release interleukins
- macrophages release chemicals that attract neutrophils by chemotaxis
- ( many cells release interferon, inhibits virus replication and stimulates t killer activity)
14
Q
Primary and secondary immune response
A
Primary
- time delay to trigger immune response after first infection
- no B memory cells so slow antibody production and few produced
Secondary
- shorter delay. Quicker response
- B memory cells are specific to the antigen of the pathogen have remained in the blood after being produced in the primary response. They can clone and differentiate to make plasma cells which make more antibodies more quickly. They give immunity to a disease.
15
Q
Groups who should be immunised
A
- elderly/ young children
- weak immune systems/ young children have had little time to build up natural immunity to many diseases
- people with HIV/AIDS
- weak immune system is can’t produce many antibodies themselves
- Pregnant women
- foetus has undeveloped immune system
- Health workers
- more likely to be at risk of getting a disease
- People with chronic diseases like TB or autoimmune diseases
- poor health and bodies may be unable to withstand further disease
16
Q
Why some people choose not to get immunised
A
- too busy or can’t be bothered to go to the doctors
- media scare stories
- concerns about side effects
- allergic to vaccine
- fear of needles
- religious reasons
- cost too expensive
17
Q
Why governments want people to be vaccinated as side from direct health benefits
A
- prevention of disease can save lost days at work by many which could harm the economy
- costs less to immunise people than to treat them
- health service wouldn’t be able to cope if large numbers of people became infected
18
Q
Why elderly and others encouraged to get a vaccine for influenza every year
A
- vaccine is changed every year
- as there are new strains of the virus each year as it has mutated from the previous year
- new strains have different antigens
- old antibodies from previous year aren’t complementary to the new antigen and the new vaccination will encourage new antibodies to be made
19
Q
How governments vaccinate people to control a disease
A
Herd vaccination
-vaccinate all at risk
-stops infection spreading if a large enough proportion is vaccinated
Ring vaccination
-requires people to report victims
-vaccinate all people living with or near the victim
-contains spread within ring
20
Q
Why it has not been possible to produce an effective malaria vaccine
A
- different strains of the proctoctist each year as it has mutated from previous year
- new strains have different antigens
- multiple stages in life cycle, each has different antigens so needs different vaccines
- plasmodium concealed in liver cells and RBCs so only exposed to immune system for a short period of time
21
Q
Why we will never know how accurate estimates of numbers of species are
A
- we will not be certain we have found all species on earth
- we are constantly discovering new species
- evolution and speciation are continuing
- many species are endangered / becoming extinct
22
Q
Why estimates of species are lower than true number
A
- not all species discovered yet
- many microscopic species are hard to see
- sampling might miss rare species
- organisms may be mistakenly identified as one when they are 2 different species
23
Q
Sampling plants
A
- set area to be sampled
- use belt transect to sample
- use 50x50 cm quadrats
- at regular 5m intervals
- identify plant species using keys
- record presence / absence
- estimate % cover
- use point frame
- repeat with several transepts to show repeatability
- use simpsons index to calculate biodiversity
- can display on a kite diagram
24
Q
Sampling animals
A
- set grid to be sampled
- use random numbers to make grid coordinates to locate areas to be randomly sampled
- appropriate method of capture ( sweep nets, pooters, pitfalls )
- identify each species with a key
- count each species
- repeat in each habitat with the same technique
- use simpsons index to calculate biodiversity
25
Q
Why classification systems change over time
A
- scientific knowledge changes as new discoveries are made
- technological developments led to new discoveries
- e.g microscopes, new DNA tech
- differences in opinion amongst scientists
26
Q
Animal features
A
- eukaryotes
- multicellular
- heterotrophic feeders
- no cell walls
27
Q
Plant features
A
- eukaryotes
- multicellular
- autotrophs
- cellulose cell wall
