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module 4 biology > disease booklet > Flashcards

disease booklet Flashcards

1
Q

why are plants useful hosts to pathogens

A
  1. supply of carbs, proteins, oils
  2. plant support transmission through seeds and fruit
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2
Q

give examples of ways plants have passive defences (present before infection)

A

cellulose cell wall
lignin thickened wall
waxy cuticle
bark (tannins)
stomatal closure
callose (in sieves, block pathogens)
tylose (swelling in xylem prevent pathogens)

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3
Q

active defences in the plant

A

oxidative bursts - cells that have pathogens can be damaged
necrosis - cell suicide
canker - sunken necrotic lesion in woody tissues = death of cambium tissue (xylem + phloem forms in meristem)

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4
Q

what is the risk of clotting?

A

blood could clot in the wrong places

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5
Q

what are histamines and what cell produce them

A

cell signalling substance
produced by mast cells

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6
Q

what events take place during inflammation?

A
  • mast cells produce histamine
  • vasodilation occurs
  • increase blood to infected area
  • capillary wall increases permeability to white BC
    -increase production of tissue fluids = swelling
    -excess tissue fluid drained into lymphatic system where lymphocytes stored
  • specific immune response
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7
Q

examples of primary defences

A

ear wax in ear canal
mucus plug in cervix + acidic conditions in vagina
antibodies and enzymes in tear fluid

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8
Q

what are opsonins

A

proteins which attack to antigenic surface of pathogen to enable phagocytosis. NOT SPECIFIC

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9
Q

main stages of phagocytosis

A
  1. detection of pathogen
  2. production of opsonins - bind to antigens of pathogen
  3. pathogen engulfed by neutrophil
  4. digestion of phagosome - lysosomes fuse with phagosome and release hydrolytic enzymes to digest
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10
Q

purpose of APC

A

macrophages present antigens on surface so SPC stops body destroying them

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11
Q

how are phagocytes specialised for their function

A

they can change their shape
lots of lysosomes to engulf phagosome
- lots of ribsomes

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12
Q

differences between macrophages and neutrophils

A

neutrophils
-smaller
-multi lobed
- made in bone marrow
- found in tissue fluid

macrophages
- larger
- round + large
- made in bone m. BUT mature in lymph nodes
- found in lymph nodes

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13
Q

differences and similarities between macrophages and neutrophils in regards to:
- form pus?
- travel in blood?
- engulf pathogens?
- form APCs?

A

differences-
PUS: N = YES M = NO
APCS N = NO M = YES

similarities-
BLOOD: N = YES M = YES
ENGULF N = YES M = YES

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14
Q

role of cytokines

A

hormone like chemicals which act as chemical messengers

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15
Q

the specific immune response can destroy pathogens using two different responses:

A

humoral - B lymphocytes outside the cell

cell mediated - T lymphocytes cell mediated response inside the cell

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16
Q

role of T helper cell

A

release cytokines which stimulate B cells to develop and stimulate phagocytosis in phagocytes

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17
Q

role of T killer cells

A

attack and kill infected body cells

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18
Q

role of T memory cells

A

provide long term immunity after the infection

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19
Q

role of T regulator cells

A

shutdown immune response once pathogen has been removed

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20
Q

role of plasma cells

A

produce antibodies

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21
Q

role of B memory cells

A

remain in body and provide long term immunity

22
Q

type of cytokines

A

monokines
interleukins
interferons

23
Q

role of monokines

A

released my macrophages, these attracts neutrophils and can stimulate B cells to divide

24
Q

role of interleukins

A

produced by T cells and macrophages, stimulate proliferation (clonal expansion) of B and T cells

25
Q

role of interferons

A

inhibit virus replication by stimulates T killer cells

26
Q

explain the process of cell mediated (T) cells

A

Cell mediated response
- macrophage engulfs pathogen and breaks in into fragments
- recombines antigenic fragments with own glycoprotein + express the antigen on its plasma membrane
- clonal selection of Th cell = secret cytokines to attract B cells
- clonal expansion via mitosis

27
Q

explain the stages of immune response in B cells (humoral)

A

-clonal expansion by mitosis
- B cells differentiate into plasma cells, which then secrete antibodies which bind to antigen and punch holes in pathogen to kill it.

28
Q

what is clonal selection

A

choosing b and T cells that are complimentary receptors to antigens of pathogens

29
Q

clonal expansion

A

process by which b and t cells undergo proliferation by mitosis indicated by interleukins

30
Q

what is an autoimmune disease

A

when immune system attacks part of the body

31
Q

give examples of autoimmune diseases

A

-lupus (swelling + antibodies attack proteins in nucleus)

-arthritis (inflammation of joints)

32
Q

Macrophages
where is it made?
how does it travel and in what state?
where does it settle?
function?
what does it release?

A
  • made in bone marrow
  • travel in blood as monocytes
    -settle in lymph nodes and organs
  • carry out phagocytosis but do not fully digest pathogen + present antigens on their surface
  • release monokines: attract neutrophils and stimulate b cell differentiation + release antibodies and interleukins
33
Q

neutrophil
where is it made?
characteristics?
function?

A
  • made in bone marrow
  • multi lobed nucleus

attracted to infected cells by the release of histamines. Travel in blood and squeeze out into tissue fluid when histamines have increased capillary permeability

  • engulf, digest + exocytosis
34
Q

plasma and memory B cell

A
  • made and mature in bone marrow
  • carry the correct receptor molecules on their membrane that is complimentary to the antigen
    -stimulated by the release of monokines from macrophages
  • plasma cells manufacture and release antibodies
  • memory cells circulate in the body providing immunological memory
  • release interleukins stimulate b and t cells
35
Q

killer and helper T cells
- where is it made/mature
- function of helper t cells
-function of killer t cells

A

made in bone marrow, mature in thymus

Th cells - release cytokines (chemical messengers) that stimulate the b cells to develop and stimulate phagocytosis

killer t cells - stimulated by interferon cause cells to rupture (lysis)

36
Q

what is the fucntion of interferons?

A

inhibit virus replication and stimulate activity of t killer cells

37
Q

what are antibodies (immunoglobins)

A

-proteins produced by plasma cells when antigen is detected
-these will bind to antigen (complimentary)
- specific primary and tertiary structure to protein allows specific shape

38
Q

what is anti-toxin

A

bind to molecules produced by pathogen which are toxic - neutralise the toxin

39
Q

lysis

A

causes rupture of bacteria cell membrane + neutralisation

40
Q

process of aglutination

A
  • plasma cells make antibodies
  • antibody binds to pathogen antigens
  • antibodies bind to multiple pathogens
  • make pathogen ineffective as it cannot evade host tissue
  • neutrophils engulf and digest many pathogens together
41
Q

describe primary response to an antigen on a graph

A

clonal selection, expansion, plasma cell production, differentiation all needs to happen which means antibody production is much slower to fight infection

42
Q

describe secondary response to an antigen on a graph

A

B and T cells already present in the blood = increase plasma cells made quickly so more antibodies are produced (clonal selection is not required second time round so immune response is quicker, soon , greater)

43
Q

immunological memory?

A

memory of our immune system

44
Q

two types of naturally acquired immunity + examples for each

A

active - antigens enter body naturally e.g. catching and recovering from a disease

passive - antibodies pass from mother to foetus

45
Q

two types of artifically acquired immunity + examples for each

A

active = antigens are introduced in vaccines e.g. taking oral vaccine for polio

passive = antibodies introduced in immune serum e.g. injection of serum containing antibodies

46
Q

two types of artifically acquired immunity + examples for each

A

active = antigens are introduced in vaccines e.g. taking oral vaccine for polio

passive = antibodies introduced in immune serum e.g. injection of serum containing antibodies

47
Q

what is a vaccination

A

stimulate the production of antibodies without causing an illness

48
Q

examples of antigenic material that can be used in vaccines.

A
  • may contain attenuated forms of pathogen
  • may contain similar but harmless forms of pathogen
  • inactive pathogen
  • harmless toxin
  • isolated pathogen
49
Q

why do we need to find new medicines

A

new emerging diseases
antibiotic resistance

50
Q

what is an emerging disease?

A

a communicable disease that has newly appeared in a population or that has rapidly increase in incidence or geographic range

51
Q

outline how bacteria are becoming resistant

A
  • bacteria shows variation, caused by mutation
  • use of antibiotics acts as selection pressure. The bacteria are resistant, survive and reproduce
    -allele for resistance will pass on to offspring which will pass on over many generations
52
Q

outline how mutation of bacteria may cause immune response to become ineffective

A

mutations cause variations
mutations are changes in base sequence DNA
- changes protein synthesis and therefore potentially the shape of the antigens
-memory cells wont recognise the pathogen. mutations could also allow the pathogen to enter host cells and hide from phagocytes, or produce additional potent toxins that prevent immune cells being able to proliferate

module 4 biology (7 decks)

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