Ch. 15 Flashcards

1
Q

What are the different stages of infection?

A

incubation stage: replication without symptoms

Prodromal stage: early s/s like fever and fatigue

acute stage: maximum manifestations, tissue damage and inflammation

convalescent stage: containment of infection, elimination of pathogen, repairing of damage

resolution stage: total elimination, no residual manifestations

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2
Q

What does itis mean?

A

inflammation

can mean virus

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3
Q

What does emia mean?

A

in the blood

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4
Q

What does sepsis or septicemia mean?

A

bacterial toxins in the blood

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5
Q

What are virulent factors and some examples?

A

things that make an infection more likely to cause disease

Toxins: endo and exo

Adhesion factors help infective organisms stick to body

Evasive factors that keep immune system from detecting

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6
Q

How do antibiotics kill bacteria? (what do they target)

A

cell wall synthesis

protein synthesis

nucleicacid synthesis

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7
Q

How do bacteria combat antibiotics?

A

inactivating antibiotics

changing antibiotic binding sites

using different metabolic pathways

changing their walls to keep antibiotics out

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8
Q

How do antivirals kill viruses?

A

block viral DNA and RNA synthesis

block viral binding to cells

block production of protein coats of new viruses

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9
Q

How many species of bacteria live in the large intestine?

A

300! WTF?!

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10
Q

Does the vagina have bacteria in it?

A

Yes, mainly acid-producing

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11
Q

What are microflora (normal flora)?

A

microorganisms that are normally living in our bodies.

  • -some useful
    • other no effect
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12
Q

What are pathogens?

A

disease causing microorganisms

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13
Q

What do opportunistic pathogens do?

A

these are microflora that are capable of causing disease if your health or immunity is weakened, making it a pathogen.

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14
Q

What are our two types of immunity?

A

innate (natural)

adaptive (acquired)

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15
Q

Is our innate immunity always present?

A

YES, we were born with it

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16
Q

Is the response of the innate immunity rapid?

A

yes, it is our first line of defense

triggers inflammation

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17
Q

Does you innate immunity distinguish between different microbes?

A

No, it only recognizes self from not self, whether it is a good or bad thing.

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18
Q

What are the mechanisms of our innate immunity?

A

epithelial barriers

phagocytic cells

plasma proteins and NK cells

cell messenger molecules

complement system

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19
Q

Do the innate and adpative immune systems work together?

A

YES

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20
Q

What are the mechanisms of adaptive immunity?

A

lymphocytes and their products

    • mediated by B and T cells
    • antibodies
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21
Q

Is adaptive immunity specific?

A

YES, it can tell different microorganisms apart

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22
Q

Does our adaptive immunity have a memory?

A

ABSOLUTELY

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23
Q

What are the two types of ADAPTIVE immunity?

A

humoral: B cells and antibodies

cell mediated: intracellular killing and T cells

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24
Q

In order for adaptive immunity to be triggered, what has to first happen?

A

Our innate immunity has to present the antigen

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25
Q

What are the specific cells of our innate immune system?

A

Phagocytic WBCs:

    • neutrophils
    • macrophages (also present antigens)
    • dendritic cells (also present antigens)

NK cells

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26
Q

What are the specific cells of our adaptive immune system?

A

lymphocytes: B and T cells

Antigen presenting cells: macrophages and dendrites

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27
Q

How are monocytes and macrophages related?

A

macrophages are mature monocytes that are found in almost all tissues

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28
Q

How long after the neutrophils do the monocytes arrive at the inflammatory site?

A

typically 24 hours or later

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29
Q

What are the functions of monocytes/macrophages?

A

phagocytosis

induce inflammation

signal proteins that activate and recruit other immune cells

general scavengers: clear out dead cells and cell debris

PART OF THE INNATE IMMUNITY(also present the antigens to activate adaptive)

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30
Q

Are neutrophils predominate in early or late inflammatory response?

A

early

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31
Q

What do neutrophils ingest?

A

bacteria

dead cells

cell debris

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32
Q

How would you describe the lifespan of a neutrophil?

A

Short

BECOME A COMPONENT OF PURULENT EXUDATE

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33
Q

Where are dendritic cells found?

A

epithelial tissue and organs (immature)

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34
Q

What do dendritic cells do?

A

capture foreign agents and transport them to regional lymph nodes (activate adaptive immunity

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35
Q

Where do dendritic cells mature?

A

lymph nodes

THIS IS WHEN THEY GET THEIR ANTIGEN PRESENTING ROLE

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36
Q

What else beside antigen presentation do the dendritic cells do for our adaptive immunity?

A

release molecules that help direct the adaptive immune system.

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37
Q

What do B cells do?

A

produce antibodies

ALSO DIFFERENTIATE INTO PLASMA CELLS THAT MAKE ANTIBODIES LIKE CRAZY

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38
Q

What do our T cells do?

A

Tell B cells to make anitbodies (CD4)

kill intracellular pathogens directly (CD8)

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39
Q

What is our first line of defense against viruses?

A

NK cells

KILL THE VIRUS WITHOUT HARMING THE HOST CELL

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40
Q

What do NK cells do?

A

1st line of defense against viruses

kill tumor cells and abnormal body cells (HUGE ROLE IN CANCER PREVENTION)

kill cells with INTRACELLULAR BACTERIA

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41
Q

What happens if the thymus releases immature T cells or T cells with faulty receptors?

A

we could get an autoimmune disorder

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42
Q

What are out central lymph tissues?

A

bone marrow and thymus

PRODUCE AND MATURE CELLS

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43
Q

What are our peripheral lymph tissues?

A

lymph nodes

spleen

MALT (like the tonsils)

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44
Q

What cells does our MALT contain usually?

A

plasma cells

CAN QUICKLY MOUNT A RESPONSE TO ANTIGENS WITH ANTIBODIES

45
Q

What does the red pulp of the spleen do?

A

removes old red blood cells

46
Q

What does the white pulp of the spleen do?

A

has a concentrations of B and T cells, macrophages, and dendritic cells, hanging out waiting to be secreted if need be. (kind of like the fire station)

47
Q

What are cytokines?

A

proteins with a short half life that are made as needed

48
Q

What do cytokines do?

A

cell to cell communicators that only act on cells with specific binding site for the cytokine

49
Q

What does it mean that cytokines and pleotropic?

A

This means that one cytokine can act on many different cell types

50
Q

What does it mean that cytokines are redundant?

A

This means that many cytokines can give out the same message or overlap duties

51
Q

Are the actions of cytokines local or systemic?

A

THEY CAN BE BOTH

52
Q

Can cytokines freely move anywhere?

A

YES, they can move without a transporter, the term for this is that they are soluble

53
Q

What are some general types of cytokines and their functions?

A

Chemokines: communicate migration and activation

CSF (colony-stimulating factors): stimulate stem cells to differentiate

54
Q

What are some specific names of cytokines?

A

interleukins

interferons

tumor necrosis factors

(many will have CSF after the name, meaning its a colony-stimulating factor)

55
Q

What are some specific epithelial barriers?

A

dead epithelial lining on outside skin, mucous, wax, cillia, enzymes released from cells of the lining of GI, respiratory and urogenital tracts

56
Q

What are the cells of innate immunity again?

A

Phagocytes: neutrophils, monocytes/macrophages, basophils, eosinophils, dendritic cells

NK cells

57
Q

What does pattern recognition mean when talking about pathogen recognition in innate immunity?

A

This just means that the innate immunity is looking for a pattern that makes it recognize the cell as not self:

a specific matrix of cell wall
organization and spacing of sugar molecules
opsonins

58
Q

What are the toll-like receptors of the innate immunity?

A

She relates it to the secret club handshake

59
Q

What are the soluble mediators of innate immunity and their functions?

A

opsonins: tag for phagocytosis

Cytokines: cell to cell communication

compliment system

60
Q

What are some physical barriers of innate immunity?

A

SKin

lining of GI, respiratory, urogenital tracts

61
Q

What are some mechanical barriers of innate immunity?

A

sloughing off of cells

coughing and sneezing

flushing (urogenital tract)

vomiting

mucus and cilia

62
Q

What are some biomechanical barriers of our innate immunity?

A

synthesized and secreted: saliva, tears, earwax, sweat, mucus

antimicrobial peptides

normal flora (compete with invaders)

63
Q

What does the MHC-1 molecule do for innate immunity?

A

This is an inhibitory receptor that tells the immune cells that it is self, stops it from getting killed

64
Q

What is dangerous about intracellular pathogens and MHC-1 inhibition?

A

The MHC-1 might not be expressed, but the intracellular pathogen isnt that harmful, the cell will be killed anyway

65
Q

What happens to the epitope (unique identification) of a cell that has been phagocytized with our innate immunity?

A

It is put on the outside of the phagocyte (antigen presentation)

66
Q

What is it and what does the complement system do?

A

Group of inactive proteins in the plasma

helps body localize, identify, and destroy infective agent

Can destroy pathogens directly

activates or collaborates with every component of the inflammatory response

67
Q

When a macrophage or a dendritic cell kills the antigen, its epitope get put on the outside of the cell, but where exactly?

A

The MHC 2 of the phagocyte

68
Q

What cells see the antigens being presented by the antigen presenting cells?

A

The CD4 cells

69
Q

After the CD4 cells see the antigen being presented by the antigen presenting cell, what are the things it can do in response to a non-self antigen?

After these processes occur that are the answer for the above question, do all of those same steps have to occur the next time we are exposed to the same antigen?

A

It can become a memory T cell so it can initiate a quicker response in the future

The CD4 cell can release cytokines to activate the B cells, the B cells then create antibodies on their surface to destroy the anitgen (the B cells go on to make memory B cells that have the specific antibodies for pathogen as well as plasma cells that pump out many free floating antibodies

The CD4 also tells the CD8 cytotoxic cell what to recognize on the inside of the pathogen, it also becomes a CD8 memory T cell, that can mount a quicker response the next time

No, a lot of these steps are skipped because of products we made in the initial exposure (we have memory cells and antibodies now)

70
Q

What is another name for antigens and what is the definition?

A

immunogens

any substance that illicits an adaptive immune response

71
Q

What are some different types of antigens?

A

microbial: bacteria, viruses, protozoa, fungi, parasites

non-microbial: pollens, animal dander, insect venom, proteins in food

72
Q

How are antigens characterized?

A

as being large and complex

73
Q

What does every antigen have identify it?

A

an epitope (unique identifier)

also have haptens that are like epitopes but on a smaller molecular basis

74
Q

What are the different cell types of the adaptive immunity and specific examples?

A

regulatory cells (control response):

    • APCs
    • T helper cells
    • T suppressor cells (suppress immune response, a way of self limiting)

Effector cells (carry out attack and eliminate antigen):

    • T cytotoxic (killer) cells
    • B cells
    • mononuclear phagocytes
    • leukocytes
75
Q

What has to happen for processing and presentation of an antigen to occur?

A

antigen must be the appropriate type

lymphocytes must be prepared to recognize the presented antigen

antigen must be appropriately presented

76
Q

Where can lymphocytes come from other than the bone marrow, specifically in a fetus?

A

The liver

77
Q

Can B cells be activated by themselves during the initial exposure to an antigen?

A

No, they have to be activated by CD4 cells initially because they havent made any antibodies yet, after initial we will have memory B cells that are always activated

78
Q

What surface proteins do the CD8 receptors attach to?

A

MHC-I

When the infected cell alter these proteins, the CD8 kills the infected cells

79
Q

What surface proteins do CD4 receptors attach to?

A

MHC-II

this will start the adaptive immune response

80
Q

What are the two types of T helper (CD4) cells?

A

Th1 - stimulate CD8 cells and other phagocyticcells to attacks the antigen

Th2 - stimulate the B cells to create antibodies against the antigen

81
Q

Do Th cells produce cytokines?

What do the cytokines do in this case?

A

YES

Inflamatory mediators - cause fever and attract WBCs to site

Growth factors - tells WBCs to divide and mature

Cell to Cell communication that controls activity of other WBCs

82
Q

What do MHC-II (major histocompatability complex) display?

A

antigens eaten by phagocytic cell, tells Th cells to start immune response

83
Q

What do MHC-I proteins do?

A

display antigens made inside an infected cell

tell CD8 cells to kill infected cell

IMPORTANT FOR INTRACELLULAR PATHOGENS (VIRUSES, AND OTHER INTRACELLULAR BACTERIA)

84
Q

Why is HLA (human leukocyte antigen) important when it comes to organ transplant?

A

The donor and recipient have to have matching HLA otherwise the recipients body will flag the new organ as not self and mount an attack against it.

85
Q

Do T cells also have antigen receptors?

A

YES

86
Q

Do the T cells have to have receptors that fit the displayed antigen in order to respond?

A

YES YES YES

87
Q

What does humoral immunity eliminate?

A

extracellular microbes

88
Q

What cells are involved in humoral immunity?

A

B cells and plasma cells

89
Q

What are the mechanisms of humoral immunity?

A

Anitgen-antibody complexes:

    • destroy by direct lysis
    • activate complement
    • activate phagocytosis
90
Q

What does cell-mediated immunity eliminate?

A

intracellular microbes

91
Q

What cells are involved in cell mediated immunity?

A

CD8 cytotoxic cells directly kill

CD4 activate macrophages (IFNy) and stimulate production of macrophages (GF)

92
Q

What are our different antibodies (immunoglobulins) and describe them?

A

IgG (circulates in body fluids, attacking antigens) CAN CROSS PLACENTA, MOST ABUNDANT FOR UNBORN BABIES

IgM (circulates in body fluids, early immune response) ACTIVATES COMPLEMENT SYSTEM, ABO ANTIBODIES IN BLOOD

IgA (found in secretions on mucous membranes; prevents antigens from entering the body) SALIVA, BREAST MILK, MUCOUS, PROTECTS FETUS WITH BREAST FEEDING

IgD (found on surface of B cells; act as antigen receptors)

IgE (found in MAST cell tissues; starts inflammation) (ALLERGIES, PARASITES, HYPERSENSITIVITIES)

93
Q

Describe the primary response of adaptive humoral immunity.

A

This is from initial exposure

There is a latent period or lag phase form the B cells needing to differentiate

94
Q

When do the IgM antibodies start attacking the antigens during the primary phase? What about IgG?

A

5 to 7 days for initial response IgM

IgG is same amount of time or slightly less as it follows the IgM response

95
Q

Describe the secondary response of adaptive humoral immunity.

A

Comes with secondary exposures

More rapid than the primary response

Larger amounts of the antibody are produced

The rapidity is because of the presence of memory cells that dont have to differentiate

96
Q

Is there more IgM or IgG during the secondary response?

A

IgG is mass produced (longer term immunity)

IgM is produced in similar quantities to the primary response

97
Q

Which humoral immune response has to do with vaccination? Boosters?

A

vaccination - primary

boosters - secondary

98
Q

Why is it important to get vaccinations 2-3 weeks before traveling?

A

This is about how long it takes for your B cells to fully differentiate into memory B cells

99
Q

Why are boosters used?

A

These can produce a secondary immune response so the body will have high IgG before even being exposed to the antigen

100
Q

What is active immunity?

A

antibodies or T cells produced after a natural exposure or immunization

LONG LASTING

101
Q

What is passive immunity?

A

preformed antibodies or T cells that are transferred from a donor to recipient (can be mother to baby, or even immunoglobulin shots)

SHORT TERM PROTECTION

102
Q

What is self regulation?

A

our immune systems way of avoiding inadequate or excessive responses

103
Q

What is self tolerance?

A

our immune systems ability to not react to self antigens

104
Q

What did she say about fetal and neonatal immunity?

A

Their antibody function is deficient:
– they can mount primary IgM response, but cant make IgG challenge

NEWBORNS HAVE IgG INITIALLY BECAUSE OF MOM, NEARLY ADULT LEVELS

105
Q

How long does the maternal IgG last in a newborn?

A

about 10 months

106
Q

How long does it take for a newborns self produced IgG to get up to normal levels?

A

about 12 months

(AS MATERNAL IS DROPPING, THE NEWBORN IS MAKING ITS OWN)

THIS IS WHY WE WAIT 12-18 MONTHS AFTER BIRTH TO GIVE VACCINATIONS

107
Q

What did she say about aging and immune function?

A

Both humoral and cell-mediated response are altered (B and T cells)

decreased production of antibodies

increased circulating antigen-antibody complexes (rheumatoid arthritis)

increase in circulating auto-antibodies

108
Q

What is the size of a normal adults thymus?

A

15% of regular size

109
Q

How are inflammation and the immune response related clinically in a physiccal exam?

A

systemic: fever (not only from immune response, pathogens can produce pyrogens), high WBC count
local: erythema, edema, warmth, exudate

Immune system triggers inflammation!