depth study Flashcards

1
Q

define leucocyte

A

white blood cells which form part of the body’s immune system, help fight infection and other diseases

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2
Q

define monocyte

A

an immune cell which becomes a macrophage or dendritic cell

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3
Q

define macrophage

A

phagocytose pathogen and secrete pro-inflammatory mediators (long-life cells)

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4
Q

define dendritic cells

A

found in tissues, boosts immune responses by showing antigens on its surface to lymphocytes to regulate adaptive immune response

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5
Q

define neutrophils

A

first immune cells to respond, travel to site of infection where microorganisms are destroyed through ingestion and releasing of enzymes, (short lived cells)

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6
Q

define Natural Killer cells

A

lymphocytes which recognise virally-infected cells as non-self via their detection of MHC complexes- able to kill tumour cells without prior activation (in contrast to cytotoxic T cells)

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7
Q

what are CD4T cells also called?

A

“helper” cells

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8
Q

What do CD4T cells do?

A

helper cells do not neutralise infections but rather trigger the body’s response to infections by stimulating other immune cells such as macrophages and B lymphocytes to fight infection

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9
Q

what are CD8T cells also known as?

A

cytotoxic T lymphocytes

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10
Q

What is the function of CD8T cells?

A

secrete cytokines which have anti-tumour and anti-viral microbial effects which ultimately result in apoptosis of the target cell

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11
Q

what is the function of interleukins?

A

interleukins are a group of proteins made by leukocytes which regulate immune responses by modulating growth, differentiation and activation during inflammatory and immune responses.

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12
Q

What does D.I.C stand for? What type of condition is it?

A

Disseminated Intravascular Coagulation; a rare but serious condition that causes abnormal blood clotting throughout the body’s blood vessels - proteins that control blood clotting become overactive

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13
Q

What does A.R.D.S stand for? What type of condition is it?

A

Acute respiratory distress syndrome; a life threatening lung injury that allows fluid to leak into the lungs, occurs when alveoli fill up with fluid, keeping your lungs from filling up with air (less oxygen reaches your bloodstream, depriving your organs of the oxygen they need to function)

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14
Q

what is anaemia?

A

not having enough healthy red blood cells to carry oxygen to the body’s tissues

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15
Q

what is a cytokine storm?

A

a life-threatening systemic inflammatory syndrome involving elevated levels of circulating cytokines and immune cell hyper-activation - this could lead to multi-organ failure and death

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16
Q

how can covid-19 trigger a cytokine storm?

A

SARS-CoV-2, the causative agent of COVID-19, attacks the immune system causing an exaggerated and uncontrolled release of cytokines which lead to anaemia or ARDS and ultimately death

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17
Q

how can a cytokine storm lead to death?

A

patients can develop ARDS as a result of acute lung damage followed by multi-organ failure and resulting in death

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18
Q

how do antiviral drugs work?

A

antivirals block receptors so viruses can’t bind to and enter healthy cells, boost the immune system to help it fight off a viral infection, lower the viral load (amount of active virus) in the body

19
Q

why do viruses mutate?

A

due to the high rate of replication, viruses are more susceptible to genetic mutations. Over time, these genetic copying errors can lead to alterations in the virus’ surface proteins or antigens which our immune system use to recognise and fight the virus

20
Q

why does virus mutation pose a problem for antiviral drugs?

A
  • antiviral drug resistance
  • increasing concern in immunocompromised patient populations, where prolonged drug exposure can lead to the selection of resistant strains
  • drugs which were originally effective will no longer be effective
21
Q

how do antiviral drug manufacturers overcome the issue of viral mutation?

A

continuous surveillance, targeting conserved regions, combination therapies (consist of multiple antiviral agents with different mechanisms of action, reduces the likelihood of viral resistance), rational drug design (design drugs which bind to regions less likely to mutate), collaboration and research

22
Q

why are viral genomes mapped?

A

to compare the viruses around now to those that were around in the past - these sequences can be used to help them decide what to include in the vaccines

23
Q

what viral diseases have antiviral drugs?

A

Influenza, Hepatitis B and C, HIV

24
Q

what are the two main antiviral drugs used in Australia?

A

Paxlovid and Lagevrio

25
Q

what is the link between anti-RNA polymerase and protein synthesis?

A

Anti-RNA polymerase disrupts the translation of the virus’ RNA in order to stop it from effectively replicating

26
Q

does SARS-CoV 2 contain DNA or RNA?

A

contains single-stranded genomic RNA

27
Q

are viruses with DNA or RNA more likely to mutate?

A

RNA - the higher mutation rates of RNA viruses can explained because RNA dependent RNA polymerases which replicate their genomes do not have a proofreading ability (unlike DNA polymerases) and are thus unable to correct mistakes during replication

28
Q

how may variants of COVID have been genome mapped to date?

A

Variants such as the alpha, beta, gamma and delta variant have been genome mapped, however new variants are constantly emerging

29
Q

What is an antibiotic?

A

Antibiotics are medicines that fight infections caused by bacteria in humans and animals by either killing the bacteria or making it difficult for the bacteria to grow and multiply.

30
Q

how do quinolones work as an antibiotic?

A

directly kill bacterial cells. Produce double-stranded breaks in the bacterial chromosome. It inhibits the DNA synthesis of bacteria by disrupting the bacterial topoisomerase type II; inhibiting the catalytic activity of DNA gyrase and topoisomerase IV (these two enzymes are critical bacterial enzymes that regulate the chromosomal supercoiling required for DNA synthesis)

31
Q

how do macrolides work as an antibiotic?

A

inhibit protein synthesis by targeting the bacterial ribosome. They do not kill bacteria, rather inhibit or suppress bacterial growth. Binds to the bacterial ribosomal subunit causing the cessation of bacterial protein synthesis. Interfere with the formation of long polypeptides and cause a premature detachment of incomplete peptide chains

32
Q

how to streptogramins act as an antibiotic?

A

interfere with the formation of long polypeptides and cause a premature detachment of incomplete peptide chains. Inhibit bacterial protein synthesis by binding sequentially to a ribosomal subunit.

33
Q

How effective are antibiotics as a treatment strategy for the control of infectious diseases?

A

They are effective at killing bacteria, however as a treatment strategy for controlling infectious disease their effectiveness is limited due to increasing resistance of bacteria to antibiotics

This is due to the drug selection pressure, which leads to the survival of a resistant bacterial population or induces antibiotic resistance mechanisms

This could lead to an incredibly resistant strain of bacteria which would be incredibly difficult to contain and control

34
Q

what is an antibody?

A

an antibody is formed for self-defence against antigens - detects harmful substances called antigens, bind to them and flag them for destruction
Y-shaped, formed of four peptide chains

35
Q

Which antibodies are thought to be a treatment for COVID-19?

A

IgG, IgE, IgD, IgM, IgA

36
Q

why are there more COVID deaths in some countries than others?

A

Lack of adequate health sector infrastructure
E.g. not enough health workers, doctors

Covid 19 death toll is 4 times higher in low-income countries than high-income countries
Not economically equipped to buy vaccines – cannot afford many vaccines

Each country has a unique health care system and combat the pandemic with varying containment and mitigation strategies → some may be more effective than others

37
Q

what is immunological memory?

A

immunological memory is when memory B and T cells generated from first infection with a pathogen can mount a more rapid and effective immune response upon reinfection

38
Q

What are naive B cells activated by?

A

T-cells

39
Q

where to B-cells move to proliferate upon activation?

A

lymphoid organs such as the spleen and lymph nodes

40
Q

how do memory B-cells activate effector T-cells?

A

by presenting antigens on MHC-II molecules

41
Q

why are memory cells quicker to proliferate?

A

as they do not require continual interaction with antigen or T-cells to survive (as they have already undergone class switching and affinity maturation) they can divide faster and produce higher affinity antibodies such as IgG in response to antigens

42
Q

What is the difference between vaccination and immunisation?

A

Immunisation = the process of becoming immune to a disease as a result of a vaccine.

Vaccination = when you receive a vaccine either by a needle or drops in the mouth.

Vaccination is the term used for getting a vaccine – e.g. having the injection or taking an oral dose
Immunisation refers to the process of both getting the vaccine and becoming immune to the disease following vaccination.

43
Q

What vaccines are currently used in Australia for Covid 19?

A

Pfizer, Oxford, Moderna, Novavax

44
Q

how are cytotoxic cells activated?

A

the CD8 receptor on the cell interacts with the MHC Class 1 molecules of other cells- if the cell is found to be non-self then the CD8T cells are activated