4.1.1 communicable disease, disease prevention and the immune system Flashcards

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1
Q

non specific defences

A

physical and chemical defences and phagocytosis

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2
Q

specific defences

A

responses producing antibodies and cytotoxic cells specific to the invading pathogen

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3
Q

examples of non specific defences

A

skin
mucus membrane
expulsive reflexes
inflammation

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4
Q

how does the skin work as a non specific defence

A

prevents entry of the pathogen
has flora of healthy micro organisms that outcompete the pathogens on body surface
produces sebum

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5
Q

what is sebum

A

oily substance that inhibits growth of pathogens

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6
Q

how does the mucus membrane work as a non specific defence

A

secrete sticky mucus
traps micro organisms
contains lysosomes which destroy bacteria and fungal cell walls
contain phagocytes

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7
Q

how does expulsive reflexes work as a non specific defence

A

coughs and sneezes eject pathogen laden mucus
vomiting and diahorrea expel contents and pathogens

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8
Q

how does inflammation work as a non specific defence

A

localised response to pathogens
mast cells are activated in damage tissues and release histamines and cytokines

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9
Q

what do histamines do

A

make blood vessels dilate causing localised heat and redness
make capillaries leaky = more plasma leaks out becoming tissue fluid = pain and swelling
dilated arterioles increase blood flow to area bringing more white blood cells
neutrophils squeeze through gaps and engulf + destroy pathogens

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10
Q

what does cytokines do

A

attract more phagocytes

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11
Q

blood clotting cascade

A

damaged tissue
platelets are activated by damaged tissue and serotonin constricts blood flow in area
thromboplastin enzyme and Ca2+ catalyses prothrombin into thrombin
thrombin catalyses formation of fibrinogen into fibrin to form the clot

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12
Q

Phagocytosis

A

microbe adheres to pathogen
phagocyte engulfs particle
phagocytotic vesicle containing microbe antigen and lysosome fuse
forms phagolysosome
microbe is killed and digested by lysosomal enzymes
indigestible material is removed by exocytosis

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13
Q

phagocytosis with antigen presenting ->
macrophage

A

phagocyte attracted by chemical produced by pathogen
phagocyte recognises pathogen as non-self + binds
phagocyte engulfs pathogen to form phagosome
lysosome binds to form phagolysosome
enzyme breaks down pathogen in phagolysosome
digested pathogen absorbed by phagocyte antigen combine with MHC in cytoplasm
MHC complex is displayed on phagocyte membrane making antigen presenting cell

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14
Q

what are opsonin’s produced by

A

B cells

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15
Q

what do opsonin’s do

A

bind to pathogen so phagocyte recognises them more easily

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16
Q

what is a cascade

A

sequence of events one after each other

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17
Q

why is high temp a symptom of many infectious diseases

A

prevent pathogen reproducing

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18
Q

Function of calcium ion in blood clotting cascade

A

cofactor for prothrombin

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19
Q

why is fibrinogen converted into fibrin

A

so it becomes insoluble and fibrous to hold the clot together

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20
Q

macrophages

A

engulf and digest pathogen except the antigen which it displays on their own cell surface membrane to become antigen presenting cell (APC)

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21
Q

why can phagocytes pass from blood into tissue fluid

A

multi lobed nucleus so can fit through leaky walls of capillary

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22
Q

parasite

A

organism that lives in a host cell to get there food from the host

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23
Q

Antibody definition

A

protein produced by white blood cells - lymphocytes that is complementary to a specific antigen

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24
Q

Antigen definition

A

protein on the surface of a cell or veins that is required by the immune system as self or non-self

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25
Q

why might a patient who receives a organ transplant is at risk of rejecting the organ

A

antigens on transplanted organ may be recognised as non self so triggers immune response

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26
Q

how to reduce risk of rejection of transplanted organs

A

give immunosuppressants to reduce immune system activity
tissue typing- check antigens compared to donors until close a match as possible

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27
Q

why are lymphocytes called lymphocytes

A

mostly live in lymph

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28
Q

B cells

A

made and develop in bone marrow
begin to produce antibodies as they mature which are placed in membrane where they’re called B cell receptors

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29
Q

once B cells are activated what do they produce

A

antibodies
carry out humoral response which help phagocyte clear up infection

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30
Q

where do t cells develop and made

A

made in bone marrow
develop in thymus gland

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31
Q

cell mediated response

A

antigen presenting cell reaches immature t cell in lymph
APC presents foreign antigen to immature t cell
APC binds to t cell with most complementary receptor to foreign antigen - clonal selection
triggers selected t cell to divide rapidly by mitosis- clonal expansion
mature T cells produced differentiate to form 4 types - t killer, helper ,regulator ,memory
t killer binds to infected body cells + destroys them by making holed in their plasma membrane
t helpers help to activate humoral response by binding to complementary immature b cell
also secrete cytokines to attract phagocytes

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32
Q

Humoral response

A

invading pathogen comes into contact with naïve b cell with complementary receptor to antigen
b cell engulfs pathogen- processes antigen to become APC
activated T helper cell binds to b cell via presented antigen- clonal selection
interleukins are produced by t helper released to activate selected b cell
b cell divides - clonal expansion
clonal b cells differentiate into plasma cells and memory b cells
plasma cells produce vast numbers of antibodies to help phagocytes clear infection
memory B cells in blood stream ready to be activated quickly if person is injected with same pathogen again

33
Q

how does vaccination make us immune to disease

A

initial antigen exposure in vaccine
primary response is launched- clonal selection, expansion and differentiation
after memory cells remain
second antigen exposure is when you are infected with real pathogen
secondary response launched - clonal selection is not needed
clonal expansion + differentiation occur
more antibodies produced quicker
no symptoms

34
Q

vaccination programmes

A

system of vaccinations and boosters that is designed to control diseases on a local, national and global scale

35
Q

who does mass vaccinations protect

A

vaccinated and unvaccinated individuals
herd immunity

36
Q

routine vaccinations

A

completed in childhood
eg MMR, polio, meningitis C

37
Q

what is a medicine

A

a chemical that can be used to treat disease

38
Q

where were medicines originally extracted from

A

plants
microorganisms

39
Q

what can medicines do

A

cure diseases
treat symptoms of disease

40
Q

personalised medicine

A

involves selecting and administering combination of drugs to patient based on their own genetic makeup
can be used to treat cancer

41
Q

synthetic biology

A

branch of biotechnology that involves redesigning biological organisms molecules and systems for medicine
involves editing existing chemical structures to make them more effective against a particular pathogen or disease eg if its become resistant

42
Q

structures of an antibody

A

binding site
hinge region
variable
constant region
disulphide bond
https://docs.google.com/document/d/1G7cBI-SBifSmuVNbZMnU1JsYktObN0CvUgXj21SRqGg/edit

43
Q

function of hinge region on an antibody

A

provides molecule with flexibility allowing it to bind to 2 separate antigens

44
Q

function of variable region on an antibody

A

different in every antibody molecule so each antibody is specific to a particular antigen

45
Q

function of constant region on an antibody

A

same on every antibody
binds to receptors on phagocytes and mast cells

46
Q

function of disulphide bonds on an antibody

A

hold chains together

47
Q

4 ways you can become immune to a disease by

A

vaccination
catching disease once and fighting it off
babies get antibodies from mothers blood and colostrum
injection of antibodies - tetanus

48
Q

immunity definition

A

ability of an organism to resist a particular infection or toxin by the action of specific antibodies or memory cells

49
Q

what are the types of immunity

A

active
passive
natural
artificial

50
Q

active immunity definition

A

having memory cells that are able to make antibodies to a particular antigen

51
Q

passive immunity definition

A

being given antibodies to a particular pathogen made by a different organism

52
Q

natural immunity definition

A

when you’re not given an injection

53
Q

artificial immunity definition

A

due to an injection

54
Q

how does passive immunity protect you against disease

A

antibodies act as opsonin’s and agglutinins and anti toxins
they bind to antigen on pathogen and phagocyte
aid phagocytosis by acting as opsonin’s and agglutinins

55
Q

how does active immunity protect you against disease

A

your cells produce memory cells

56
Q

when does primary immune response occur

A

when you’re first exposed to a pathogen
vaccine or catching the disease

57
Q

what does the primary immune response involve

A

full cell mediated and humoral response

58
Q

why is the primary immune response slower

A

there’s no previous immunity or memory cells

59
Q

what are the 3 main stages of cell mediated and humoral response

A

clonal selection
clonal expansion
differentiation

60
Q

how do memory cells work

A

they continue to secrete a small amount of high affinity antibodies

61
Q

immunological memory

A

memory cells secreting high affinity antibodies

62
Q

when does the secondary immune response occur

A

when you get exposed to the pathogen for a second time

63
Q

what happens when the body is exposed to the same antigen again

A

low levels of free antibodies are in the blood and bind to the antigens on the pathogens
triggers T and B cell response

64
Q

why are T and B cells activated quicker in secondary response

A

clonal selection doesn’t need to occur

65
Q

difference between primary and secondary antibody response

A

secondary is faster and produces a higher concentration of antibodies

66
Q

how do antibodies to measles come present in children at birth

A

from the blood shared in the placenta from the mother

67
Q

type of cell that produces antibodies

A

B cells

68
Q

autoimmune disease

A

immune system stop recognizing “self” cells and starts to attack healthy body tissue

69
Q

what does autoimmune disease result in

A

causes chronic inflammation or complete breakdown and destruction of healthy tissue

70
Q

what is a treatment of autoimmune diseases

A

immunosuppressant drugs to prevent immune system from working

71
Q

3 autoimmune diseases

A

type 1 diabetes
rheumatoid arthritis
lupus

72
Q

body part affected and treatment of type 1 diabetes

A

insulin secreting cells of pancreas
treatment= insulin injections
pancreas transplants
immunosuppressant drugs

73
Q

body part affected and treatment of rheumatoid arthritis

A

joints in hand, wrists, ankle, feet
treatments = no cure
anti-inflammatory drugs
steroids
immunosuppressants
pain relief

74
Q

body part affected and treatment of lupus

A

affects skin and joints and causes fatigue
can attack any organ in the body including kidney, liver, lungs or brain

75
Q

what do antibodies do

A

make process of phagocytosis faster and more efficient
destroy toxins produced by bacteria

76
Q

what can antibodies act as

A

opsonin’s
agglutinins
antitoxins

77
Q

what do opsonins do

A

make complex easier to be engulfed and digested
bind to pathogen via antigen and acts as tag

78
Q

what do agglutinins do

A

cause pathogen carrying antigen- antibody complexes to clump together preventing them from spreading to body so phagocyte can engulf more at a time

79
Q

what do antitoxins do

A

neutralise toxins - toxins released by bacteria
bind to toxin and neutralise it preventing them from binding to the cell and causing damage