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HSC Biology > Module 7 - Depth Study > Flashcards

Module 7 - Depth Study Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

monocytes

A
  • type of WBC formed in bone marrow
  • turn into macrophage or dendritic cell after moving from bloodstream into tissues in response to infection
  • mac + dend are APCs (participate in acquired immunity)
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2
Q

neutrophils

A
  • first to move to site of infection to inactivate pathogens
  • produce neutrophil extracellular traps to bind + trap pathogens, preventing further spread
  • recruits other immune cells to SOI but not APCs (self-destruct after a few days)
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3
Q

leukocytes =

lymphocytes =

A

WBCs

type of leukocyte

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4
Q

NK cells

A

innate immune system

  • don’t attack pathogens directly but destroy infected host cell
  • cytotoxic - contain cytoplasmic granules filled with perforin + proteases
  • once it detects a ‘non-self’ cell it attaches to it + releases these cytotoxic molecules causing the lysis (rupture) + death of target cell
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5
Q

Dendritic cells (DC)

A
  • presents antigens on surface (APCs) - located in tissues - common points for infection - triggers adaptive immune response
  • messenger between the innate and adaptive immune system
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6
Q

CD4T

A

‘helper’ T cells - they do not neutralise infections but rather trigger the body’s response to infections

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7
Q

CD8T

A

adaptive immune system

  • during an infection, naïve CD8+ T cells are initially stimulated by interacting with APCs within lymphoid organs
  • CD8T cells are cytotoxic T cells that induce cell death either by lysis or apoptosis
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8
Q

Interleukin (IL)

A
  • naturally occurring proteins that mediate communication between cells
  • can elicit many reactions in cells and tissues by binding to high-affinity receptors in cell surfaces
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9
Q

cytokine

A

small, short-lived proteins (made in response to pathogens)

  • released by one cell to regulate the function of another cell, thereby serving as intercellular chemical messengers
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10
Q

D.I.C.

A

Disseminated Intravascular Coagulation = implication of Cytokine Storm

  • a serious disorder in which the proteins that control blood clotting become overactive
  • abnormal clumps of thickened blood clots form inside blood vessles (use up clotting factors) –> can lead to massive bleeding in other places
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11
Q

A.R.D.S.

A

Acute respiratory distress syndrome = CS can cause ARDS

  • a serious lung condition that causes low blood oxygen
  • fluid buildup and break down of surfactant prevent the lungs from properly filling with air and moving enough oxygen into the bloodstream and throughout the body
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12
Q

Anaemia

A
  • condition where the # of RBCs or haemoglobin concentration within them is lower than normal

–> decreased capacity of the blood to carry oxygen to the body’s tissues

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13
Q

Cytokine storm

A
  • excessive, uncontrolled immune response characterised by a widespread release of many pro-inflammatory cytokines

–> overactivation of other immune cells like T-cells, macrophages, and natural killer cells
–> (can) tissue damage, organ dysfunction, and sometimes death

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14
Q

how antiviral drugs work

A

Rather than killing a virus directly, antivirals usually inhibit the growth, development and multiplication of viruses at different points

  • anti-entry
  • protease inhibitors
  • anti-RNA polymerase
  • anti-viral release

= do not cure the disease but slow down the progress allowing the body’s natural defences to take over

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15
Q

why viruses mutate

A

all organisms mutate (natural selection)

  • by becoming more effective in moving from host to host + reproducing faster, a virus can extend its life
  • mutation can help viruses evade immune responses + vaccines + antivirals
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16
Q

why virus mutation problem for antivirals

A
  • viruses have high mutation rates
  • mutation might give virus antiviral resistance to a drug = certain antiviral has lower effectiveness in inhibiting the spread + harm of a particular virus
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17
Q

reasons viruses are genome-mapped

A
  • help to track the way a virus is spreading + changing
  • easier to develop vaccines (don’t need actual sample)
  • compare current and past viruses
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18
Q

viral diseases with antiviral drugs (6)

A
  • coronaviruses, e.g. COVID-19
  • ebola
  • flu
  • genital herpes
  • hepatitis b and hepatitis c
  • HIV
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19
Q

two antiviral drugs for COVID-19 in Australia

A

primarily used for people with mild COVID-19 who have a high risk for developing severe disease, reducing the need (or lowering the risk) for admission to hospital

oral:
* Paxlovid (most effective oral treatment to date)
* Lagevrio (molnupiravir)

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20
Q

covid - rna or dna virus?

A

RNA

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21
Q

RNA viruses vs DNA viruses - mutate

A
  • RNA viruses - replicate using RNA polymerase which doesn’t proofread + makes many mistakes (generally no error correction ability) = mutations accumulate rapidly
  • DNA viruses - replicate using DNA polymerase which do proofread + have cell repair mechanisms = much lower chance of mutating
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22
Q

reverse transcriptions

A

synthesis of DNA from an RNA template

RNA is starting material

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23
Q

link between Anti-RNA polymerase and protein synthesis

A
  • Anti-RNA polymerase refers to substances or molecules that inhibit the activity of RNA polymerase –> disrupts/halts transcription –> decrease/absence of mRNA synthesis
  • reduction/absence of mRNA molecules prevents translation –> disrupts protein synthesis
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24
Q

of variants genome mapped to date

A

13

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25
Q

covid variants

A

Alpha, beta, gamma, delta, omicron

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26
Q

antibiotic define

A

A chemical substance, generally produced by a microorganism, that kills bacteria or slows its growth

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27
Q

different classes of antibiotics

A
  • quinolones
  • macrolides
  • streptogramins
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28
Q

bacteriostatic vs bactericidal antibiotics

A
  • Bacteriostatic antibiotics: slows growth of bacteria by interfering with processes the bacteria need to multiply, e.g. DNA replication, protein production, etc.
  • Bactericidal antibiotics: kill bacteria, e.g. by preventing bacteria from making a cell wall, cell membrane or its cell contents
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29
Q

quinolones - bacteriostatic or bactericidal?

A

bactericidal

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30
Q

macrolides - bacteriostatic or bactericidal?

A

bacteriostatic

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31
Q

streptogramins - bacteriostatic or bactericidal?

A

bactericidal

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32
Q

gram + vs gram -

A
  • refers to the classification of bacteria by the colour they turn in the staining method
  • gram + has thick peptidoglycan cell wall, more susceptible to antibiotics that target the cell wall BC higher permeability with no outer membrane
  • gram - has thin peptidoglycan cell wall, more resistant to antibiotics BC complex cell wall + has outer membrane (selective permeability)
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33
Q

quinolones - research and effectiveness

A
  • interfere with bacteria DNA (!!!) replication + transcription (inhibit bacteria’s ability to grow/infect cells in body)
  • broad-spectrum antiobiotic
  • quite effective against gram-negative bacteria (e.g. E. coli)
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34
Q

quinolones examples

A
  • ciprofloxacin - treat people exposed to anthrax / certain types of plague
  • levofloxacin - treat pneumonia, UTIs, sinus infections
  • trovafloxacin - treat pneumonia, abdominal infections, etc.
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35
Q

macrolides - research and effectiveness

A
  • prevents bacteria from producing proteins they need to grow + multiply (done by binding to the 50S subunit of the ribosome)
  • relatively poorly absorbed orally; used for infections caused by gram-positive bacteria
  • often used to treat people allergic to penicillins
36
Q

macrolides examples

A
  • erythromycin - used to treat bronchitis, pneumonia, whooping cough
  • clarithromycin - used to treat pneumonia, cellulitis, ear infections, etc.
37
Q

streptogramins - research and effectiveness

A
  • inhibits the synthesis of proteins by bacteria by binding to the 50S ribosomal subunit
  • mainly effective against gram positive bacteria
  • streptogramin A and streptogramin B (separately are bacteriostatic, together are bactericidal)
38
Q

streptogramins examples

A

pristinamycin IIA, pristinamycin IA

  • reduced risk of drug resistance
39
Q

broad vs narrow spectrum antibiotics

A
  • Broad spectrum = affect many different bacteria in the body including useful bacteria in the gut (implication)
  • Narrow spectrum = only affecting 1-2 types of bacteria
40
Q

important features of a bacterial cell

A

Plasmid, cell wall, cell membrane, genetic material, cytoplasm, ribosomes

If asked to draw, remember to draw pili!

41
Q

effectiveness of antibiotics as a treatment strategy for control of infectious diseases

A
  • when used correctly = highly effective
  • antibiotic resistance (overuse or bacteria mutation) –> less effective
42
Q

antibodies define

A

(immunoglobulin)

a type of blood protein naturally produced by B cells in response to a specific antigen, and play a critical role in the immune system’s 3rd line of defence, with the function of neutralising the pathogen

43
Q

which antibodies treat COVID-19?

A

IgG

IgA

44
Q

the big fancy pentagonal antibody

A

IgM

45
Q

the antibody with the secretory protein

A

IgA

46
Q

IgG
(1) location in body
(2) percentage in body/plasma

A

(1) Found mainly in blood + tissue fluids

(2) 75-80%

47
Q

IgG function

A
  • provide long-term resistance to disease - level of IgG is raised in body after booster injection of vaccine
  • can cross placenta and provide immunity to foetus and child up to age of 6 months
48
Q

IgE
(1) location in body
(2) percentage in body/plasma

A

(1) Skin, lungs + mucous membranes

(2) 0.02%

49
Q

IgE function

A
  • in the presence of specific antigens, binds to high-affinity receptors (located mostly on basophils + mast cells) and low-affinity receptors (B cells, T cells, etc)
  • binding sets off chain reaction –> causes cells to release chemical immune mediators (e.g. histamines)
  • allergic reaction + fights parasitic infections
50
Q

IgD
(1) location in body
(2) percentage in body/plasma

A

(1) Found on the surface of B cells (part of the B cell receptor)

(2) 1%

51
Q

IgD function

A

Effective against toxins and allergens + stimulates B lymphocytes to secrete other immunoglobulins

52
Q

IgM
(1) location in body
(2) percentage in body/plasma

A

(1) Blood + lymph fluid

(2) 7%

53
Q

IgM function

A
  • First to appear (when B lymphocytes are stimulated) + produce primary immune response
  • IgM levels decline as the body starts producing more IgG antibodies, which are responsible for long-term protection against pathogens
54
Q

IgA
(1) location in body
(2) percentage in body/plasma

A

(1) Found in tears, saliva, seminal fluid, urine, mother’s milk and colostrum

(2) 10-13%

55
Q

IgA function

A

Provides first line of defence against inhaled and ingested pathogens + fight against invading microbes even before the person is sensitised

56
Q

Australia vaccine rollout

A
  • people are worried about the Oxford/AstraZeneca vaccine causing blood clots = innoculation process glacial pace
  • Atagi changing vaccination advice several times: Pfizer ‘preferred’ vaccine for under 60s –> all adults >18 vaccinated, incl. AstraZeneca if need be
57
Q

reasons for more deaths in some countries than others

A
  • Lack of public health infrastructure and facilities: not enough doctors, hospitals, equipment especially in ICU
  • Lack of systemic testing, social distancing guidelines, public education
  • Quantity + success of vaccination rollouts
  • Level of pre-COVID income inequality: for those who earn a much lower income, quarantining/social distancing is not a viable option (especially if it is not mandatory)
58
Q

covid deaths by year

A

2019: 0
2020: 1,946,419
2021: 3,531,717
2022: 1,238,166
2023: 219,587

1.9m, 3.5m, 1.2m, 0.2m

59
Q

secondary immune response

A
  1. upon meeting their SPECIFIC antigen again, memory cells rapidly proliferate + differentiate into plasma cells
  2. plasma cells produce abundant quantities of antibodies to clear the antigen
  3. some memory cells sent to germinal centres for further affinity maturation + class changeover
60
Q

primary vs secondary immune response

A
  • primary: curve flatter + shorter because it takes some time for naive B and T cells with the appropriate antigen specificities to be identified, activated and then proliferate
  • secondary: upon reinfection, memory memory B cells recognise the antigen and quickly differentiate into plasma cells, outputting ten to hundred-fold greater antibody amounts than the number that were secreted during the primary response

no. of antibodies after secondary immune response > after primary immune response

61
Q

main type of antibody produced during primary immune response

A

mainly IgM (although small amounts of IgG are usually also produced)

62
Q

main type of antibody produced during secondary immune response

A

IgG (although small amounts of IgM are sometimes produced)

63
Q

vaccination vs immunisation

A
  • vacc: term used for getting the vaccine, either injection or oral dose
  • immun: process of getting vaccinated AND being immune to the disease following vaccination
64
Q

the different COVID vaccines (5)

A
  • Pfizer Bio N Tech
  • Oxford AstraZeneca
  • Janssen/Johnson & Johnson
  • Novavax
  • Moderna
65
Q

types of COVID vaccines (3)

A
  • mRNA
  • vector
  • protein subunit
66
Q

COVID mRNA vaccines

A
  • Pfizer Bio N Tech
  • Moderna
67
Q

COVID protein subunit vaccines

A
  • Novavax
68
Q

COVID vector vaccine

A
  • Oxford AstraZeneca
  • Janssen/Johnson & Johnson
69
Q

how mRNA vaccines work

A
  • mRNA with instructions for making S protein on COVID-19 virus surface developed in lab
  • after vaccination, muscle cells begin making S protein pieces and display them on cell surfaces → body produces specific antibodies = bind to virus upon reinfection (stops it replicating)
  • once the protein pieces are made, the cells break down the instructions and get rid of them
70
Q

how vector vaccines work
for COVID-19

A
  • Material from the COVID-19 virus is placed in a modified version of a different virus (viral vector)
  • Injected: viral vector gives cells instructions to make copies of the COVID-19 S protein
  • Once cells display the S proteins on their surfaces, the immune system responds by creating antibodies and defensive white blood cells = fight virus upon reinfection

NOTE: Viral vector vaccines can’t cause you to become infected with the COVID-19 virus or the viral vector virus

71
Q

how protein subunit vaccines work

for COVID-19

A
  • spike protein material removed from virus + inserted into bacteria, yeast or animal cells
  • COVID-19 virus spike protein produced by cells + purified + combined with substances to boost immune response
  • injected –> spike protein created in muscle cell, recognised by immune system, produces antibodies which bind to virus + stop it from replicating if reinfected
72
Q

vaccines currently used in Australia for COVID-19

A
  • Comirnaty (Pfizer)
  • Spikevax (Moderna)
  • Nuvaxovid (Novavax)
73
Q

types of traditional vaccines (in general) - 6

A
  • live-attenuated
  • toxoid
  • inactivated
  • recombinant
  • sub-unit
  • conjugate
74
Q

live-attenuated vaccines - definition and example

A

use weakened (attenuated) form of the germ that causes the disease –> strong, long-lasting immune response

e.g. measles

75
Q

toxoid vaccines - definition and example

A

use toxoids as antigens - immune response targeted to toxin instead of the whole germ

the disease in this case is caused by the toxin secreted by the bacteria

e.g. tetanus

76
Q

inactivated vaccines - definition and example

A

use the killed version of the germ that causes a disease - protection not as strong as live vaccines

e.g. rabies

77
Q

recombinant vaccines - definition and examples

A
  • only uses proteins of a virus to activate the immune system
  • proteins made via genetic engineering by cells that use recombined pieces of the viral genetic code to churn out proteins
  • proteins injected in person = activate immune system
  • e.g. Hepatitis B
78
Q

sub-unit vaccines - definition and examples

A
  • only uses very specific subunits of a pathogen to cause a strong immune response to key parts of the pathogen
  • booster shots needed for ongoing protection
  • e.g. Hepatitis B
79
Q

conjugate vaccines - definition and examples

A
  • made by chemically linking a protein molecule with a tiny amount of the polysaccharide that makes up the cell coating of the bacterium
  • combines a weak antigen with a strong antigen as a carrier so that the immune system has a stronger response to the weak antigen

e.g. Hepatitis B

80
Q

what does lysosome do in adaptive immunity?

A
  • after phagocytosis, lysosomes in the macrophage break down the pathogen/antigen into parts
  • one of those parts is used to display on the MHCII molecule on the macrophage
81
Q

PAMPs vs DAMPs

A

PAMPs

  • molecules associated with pathogens (not presented in host cells) - often repetitive structures

DAMPs

  • endogenous (internal cause) molecules released / exposed when cells undergo stress, injury or damage
82
Q

what happens to viruses if they don’t have protease?

A

viral cells are unable to self-replicate, and this results in a low viral load

83
Q

why do viruses need protease?

A

need protease to develop + mature

  • in viral replication, viruses produce large precursor proteins which aren’t fully functional in long form
  • viral proteases recognise specific points along precursor proteins, cut them and it becomes smaller, functional pieces which be assembled into new infectious particles
84
Q

the cool thing about dimeric IgA

A

additional ‘secretory protein’ = helps antibody from being digested by enzymes (because it exists in high enzyme areas e.g. saliva and tears)

85
Q

class switching antibody production

A

B cells can change the type of antibody they produce while maintaining specificity for the same antigen

  • B cells start by making IgM antibodies but can switch to making other classes
  • Done by reorganising the DNA within the B cell to activate a different antibody gene segment
86
Q

allergies + antibodies

A
  • The first time an allergy prone person encounters an allergen, a large amount of specific IgE antibodies are produced + attach themselves to mast cells (which contain histamines)
  • When allergen is encountered again, the antibodies created after the first exposure bind to it, alerting the immune system that it needs to be destroyed
  • But in an allergy response, when the immune system destroys the allergen, it also destroys the mast cells which causes it to release its histamine = allergic response (sneezing, wheezing, sniffling)
  • Subsequent exposure to allergens are usually worse
87
Q

interferon

A

a cytokine that inhibits viral replication

HSC Biology (12 decks)

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