Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Wrong Exam Qs > disease🦠 > Flashcards

disease🦠 Flashcards

1
Q

in phagocytosis, when the bacteria is engulfed, how are its antigens removed for APC

A

in the phagosome the bacteria is partly broken down by lysozyme so antigens still whole

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

how are correct t helper cells selected

A

receptors on plasma membrane of t helper cell are complementary to antigen

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

explain importance of b memory cells in immunity

A
  • produced in primary immune response
  • remain in body
  • produce secondary immune response
  • quickly before symptoms occur
  • divide into plasma cells
  • to rapidly produce antibodies
  • long term immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the action of phagocytic cells at site of infection

A
  • pathogen recognised as foreign
  • binds to antigen
  • phagocytosis/ pathogen engulfed
  • forming phagosome
  • lysosomes fuse to phagosome forming phagolysosome
  • release enzymes to digest pathogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where are b and t lymphocytes made and where do they mature

A

b lymphocytes- made in bone marrow, mature in bone marrow

t lymphocytes- made in bone marrow, mature in thymus gland

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

describe the changes that occur to t lymphocytes during an immune response. explain the roles of t lymphocytes in fighting a pathogen

A
  • t cell with complementary receptors to antigen is selected for
  • by clonal selection
  • this t cell undergoes clonal expansion
  • t helper cells release cytokines
  • to stimulate b cells to differentiate into plasma cells
  • to stimulate macrophages to carry out phagocytosis more actively
  • t killer cells kill infected host cells
  • secrete enzymes
  • t memory cells stay in body to provide long term immunity
  • secondary immune response if reinfected, rapid response
  • active immunity

-cell mediated response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is parasite

A
  • lives in host
  • gains nutrients from host
  • at expense of host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does plasmodium bypass human primary defence

A
  • mosquito feeds on blood

- breaks skin so cannot act as barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

why is malaria common in tropical areas

A

suitable climate for mosquito

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why are erythrocytes that contain plasmodium more likely to be engulfed by phagocytes than healthy erythrocytes

A

different chemicals that attract phagocytes are released from infected erythrocytes

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

describe how structure of antibody allows them to perform function

A
  • 4 polypeptides 2 light chains 2 heavy chains
  • variable region allows binding to antigen
  • 2 variable regions allow binding of more than one antigen
  • variable region on different antibodies allows specificity to different antigens
  • constant region allows binding to phagocytes
  • hinge region allows flexibility
  • disulfide bonds hold polypeptides together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do antibodies neutralise

A
  • prevent binding to host cell
  • block antigen of pathogen
  • bind to toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

explain agglutination of antibodies

A
  • clump together many pathogens
  • so phagocyte can engulf many pathogens at once
  • clump too large to enter host cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why is saying that bacteria are immune to antibiotics incorrect

A
  • do not have immune system
  • resistant
  • bacteria are unicellular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why are phagocytes described as the secondary defence

A

-involved after pathogen has entered body

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

why are phagocytes considered non specific

A

-able to digest many different pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do phagocytes pass from blood into tissue fluid

A
  • lobed nucleus so cell can change shape
  • can move through pores in capillary walls
  • histamine makes capillary walls leaky
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

infective agent that causes tuberculosis

A

M.tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does tuberculosis pathogen spread

A
  • droplets
  • cough
  • inhaled by individuals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

factors that increase TB infection

A
  • overcrowding
  • poor diet
  • homelessness
  • not vaccinated due to no access
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how does mosquito transmit malaria to human

A
  • mosquito is vector
  • plasmodium present in mosquito saliva
  • infected mosquito bites human
  • plasmodium passes from saliva to blood
22
Q

which lymphocytes secrete substances to kill infected cells

A

-T

23
Q

which lymphocytes activate other lymphocytes

A

T

24
Q

why is influenza vaccine changed every year

A
  • different antigen shape
  • mutates
  • antibody produced needs to match new strain
25
Q

difference between primary and secondary immune response

A
  • secondary starts earlier
  • secondary more rapid
  • secondary produces more antibodies
26
Q

role of memory cells

A
  • recognise pathogen
  • produce clones
  • B memory cells divide into plasma cells which produce antibodies
  • T memory cells differentiate into T killer cells which kill infected host cells
  • pathogen killed before symptoms
27
Q

drug which inhibits viral enzyme that allows it to leave host cell- how does drug reduce spread of virus

A
  • virus cannot leave host cell
  • fewer viruses produced
  • cannot infect other cells
28
Q

why would drug researchers focus on plants used in traditional medicine

A
  • already identified medicinal properties
  • reduces time in finding active chemicals
  • reduces cost
29
Q

how does reverse transcriptase allow virus to take over cell

converts rna into dna

A
  • reverse transcriptase in nucleus
  • viral DNA inserted into host DNA
  • so viral RNA is transcribed
  • to code for viral proteins
30
Q

how do cytokines stimulate specific groups of B cells to divide

A
  • cytokine has specific shape
  • cytokine is complementary to receptor on b cell
  • cytokine binds to receptor
  • activates clonal expansion
31
Q

primary defence

A
  • skin prevents entry of pathogens
  • tears kill bacteria
  • mucus traps pathogens
32
Q

how is vaccination active

A

body produces antibodies and lymphocytes are activated

33
Q

why do you need different vaccines for different pathogens

A
  • each pathogen has different antigen
  • antigens have specific shape
  • antibodies are complementary to antigen
  • different antibody needed for each pathogen
34
Q

difference in primary and secondary immune response

A

primary is slower due to clonal selection and expansion

secondary is quicker due to memory cells

35
Q

what type of pathogen is ring rot

A

bacteria

36
Q

what type of pathogen is potato blight

A

protoctist

37
Q

what type of pathogen is black sigatoka

A

fungi

38
Q

what type of pathogen is ring worm

A

fungi

39
Q

passive plant defences against pathogens

A
  • bark
  • casparian strip
  • tannins (enzyme inhibitor on surface)
  • waxy cuticle
  • cellulose cell wall
  • resin in bark
  • toxic compounds
40
Q

active plant defences against pathogens

A
  • hypersensitivity (rapid death of tissue surrounding infection)
  • release of callose and lignin, deposited between plasma membrane and cell wall forms barrier
  • callose helps narrow plasmodesmata
  • sieve plates blocked with callose
  • callose grows into xylem
41
Q

cell signalling in plant defence

A
  • pathogens break down cell wall with cellulase
  • molecules produced in this breakdown act as cell signalling molecules and trigger receptors
  • triggering of receptors cause release of phytoalexins
  • plants under attack secrete ethene from leaves
  • ethene vaporises and stimulates other leaves and plants to react
  • salicylic acid migrates to uninfected area
  • then activates defence mechanism
  • systemic acquired resistance
42
Q

role of phytoalexins

A
  • disrupt pathogen metabolism
  • delay pathogen reproduction
  • disrupt bacteria plasma membrane
  • stimulate release of chitinases
43
Q

meningitis pathogen name

A

N. meningitidis

44
Q

direct vs indirect transmission

A

direct- from host to host

indirect- by a vector

45
Q

second line of defence in humans

A
  • phagocytosis
  • blood clotting
  • inflammation
  • wound repair
46
Q

describe blood clotting

A
  • platelets come into contact with collagen from wall
  • platelets stick together to form temporary plug
  • platelets release thromboplastin which converts prothrombin in thrombin
  • thrombin converts fibrinogen into fibrin
  • fibrin forms mesh which traps blood cells to form clot
47
Q

what happens in inflammation

A
  • increased blood flow and phagocytes move into tissue
  • mast cells secrete histamine
  • histamine causes vasodilation, leaky capillaries, phagocytes leave blood, release of cytokines
48
Q

what is chemotaxis

A

neutrophils attracted to site of infection by chemical stimuli

49
Q

what are macrophages

A
  • larger than neutrophils
  • travel in blood as monocytes and settle in tissues as macrophages
  • become APC
50
Q

what is opsonisation

A

antibody binds to pathogen to make it easily identifiable to phagocytes

51
Q

types of vaccine

A

live attenuated and inactivated

Wrong Exam Qs (41 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions