Microbio Exam #4 Ch. 15 Flashcards

(94 cards)

1
Q

Innate immunity characteristics

A

first line of defense
immediate response
not specific
present before birth
always on (infection, incubation, after infection ends)

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2
Q

adaptive immunity characteristics

A

specific to target
slow to activate
must “see” the antigen
generates memory cells

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3
Q

all immune cells stem from

A

hematopoeticprecursor stem cells from bone marrow

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4
Q

WBC for Innate Immunity

A

polymorphemic leukocytes, monocytes, macrophages, dendritic cells, and mast cells

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5
Q

types of polymorphemic leukocytes

A

eosinophils, neutrophils, and basophils

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6
Q

neutrophil characteristics

A

make up almost all WBC in blood
engulfs microbes by phagocytosis

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7
Q

basophil and eosinophil characteristics

A

phagocytose less efficiently than neutrophils
release toxic products to microbiome
vasoactive chemical mediators important for inflammation
they are APC (present antigens to T cells)

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8
Q

mast cell characteristics

A

contains granules rich in histamine and heparin
resides in connective tissue and mucosa
doesn’t circulate in bloodstream

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9
Q

myeloblasts give birth to

A

eosinophils, basophils, neutrophils

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10
Q

monocytes give rise to (what types of cells are the babies)

A

dendritic cells and macrophages

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11
Q

monocyte characteristics

A

circulate in blood
breaks into macrophage and dendritic cells
agranulocytes

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12
Q

macrophage characteristics

A

widely distributed throughout the body
phagocytose
“present” antigens on cell surface to T cells

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13
Q

dendritic cells characteristics

A

located in spleen, lymph nodes, and Langerhans cells in skin
phagocytose
“present” small antigens on their cell surface to T cells
different from macrophages in structure

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14
Q

high eosinophils is usually a sign of what type of infection?

A

allergy or parasitic

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15
Q

phagocytosis step 1

A

bacterium binds to the surface of phagocytotic cell. Antibody or complement can aid binding

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16
Q

phagocytosis step 2

A

phagocyte pseudopods extend and engulf the organism

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17
Q

phagocytosis step 3

A

invagination of phagocyte membrane traps the organism within a phagosome

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18
Q

phagocytosis step 4

A

lysosome fuses and deposits enzymes into the phagosomes. enzymes cleave macromolecules and generate reactive oxygen, destroying the organism

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19
Q

What is a WBC differential

A

test that measures the percent and absolute number of each type of WBC in blood

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20
Q

Neutrophils can be reduced in what kind of infection??

A

viral infection

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21
Q

What causes an increase in monocytes

A

chronic infections (TB, rickettsiosis, subacute bacterial endocarditis, etc.)

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22
Q

Primary lymphoid organs characteristics

A

Where immature lymphocytes mature
Bone marrow (B-cell)
Thymus (T-cell)

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23
Q

PMNs and mast cells are

A

granulocytes

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24
Q

eosinophils elevated when

A

parasitic and allergy

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25
basophils are elevated when
allergy
26
lymphocytes elevated
viral infection
27
secondary lymphoid organs parts
lymph nodes, spleen, peyer's patches (small intestine), tonsils, adenoids, appendix
28
T cells and B cells are what kind of immunity
adaptive
29
What are types of physical barriers to infection
skin, mucous membranes, lungs
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What makes skin a good physical barrier to infection?
protective shield covered with keratin sebum covers and protects skin (acidic pH stops bacteria) competition between species limits colonization constant shedding SALT and Langerhans cells
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what is antagonism
competition for foreign microbes on our skin
32
What is SALT/Langerhans cells and how does it help stop infection
recognizes microbes that may slip past the physical barrier and Langerhans cells (specialized dendritic cells) can phagocytize microbes
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What makes mucous membranes a good physical barrier
selectively permeable barrier against invading pathogens coats surfaces and traps microbes (lysozyme and lactoperoxidase) MAMPS mucosa associated lymphoid tissue (MALT) gut associated lymphoid tissue (GALT) Peyer's patch M cells (specialized cells that take up microbes from intestines)
34
what are MAMPs
pieces of microbes that the immune system recognizes as "foreign" types: lipopolysaccharides (gram-negative) and peptidoglycan (bacteria cell walls) recognized by toll and nod receptors
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what are MALT
Mucosa associated lymphoid tissue (GALT is a special type of MALT)
36
what is GALT
gut associated lymphoid tissue (lymph nodes, peyers patches, etc.)
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What can lymph nodes be used for?
gathering spots for dendritic cells and sites for antigen presenting cells
38
What makes the lungs a good physical barrier
cilia that line the nasal cavity sneezing clearing the organism out respiratory mucociliary elevator organisms that get to alveoli are met by phagocytic cells (alveolar macrophages) who ingest/kill and send out signals to attract immune system cells
39
what are the chemical barriers to infection
acidic pH of stomach lysosome found in mucus and tears (degrades G+ cell wall) superoxide radicals can be generated by host (dangerous for protein folding and enzyme interactions) defensins
40
what are defensins
small cationic peptides that produce pores in bacterial membrane (skin, lungs, etc.) destroys microbial membranes effective against some G+, G-, fungi, viruses **bacteria have slight negative charges**
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What is SHARP
5 signs of inflammation Swelling, Heat, Altered functions/loss of function, Redness, Pain
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what does inflammation lead to/response
phagocytic cells (neutrophils) enter infected areas within tissue, extravasation (defense system)
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extravasation
movement of WBC out of blood vessels to site of infection
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Steps of acute inflammation
infection, macrophages (release of inflammatory mediators, vasoactive factors, phagocytosis, and cytokines), then extravasation (vasodilation)
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What are vasoactive factors?
molecules that alter blood flow and endothelial permeability can result in vasodilation released by macrophages
46
Vasoactive factors medicine examples
leukotrienes, platelet-activating factor, prostaglandins, histamine
47
what does vasodilation do?
slows blood flow and increases blood volume in the affected area paired with extravasation, produces SHARP
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what do cytokines do (inflammation)
released by macrophages communicate with other cells controls inflammation and mounts a response
49
Acute inflamation characterisitcs
caused by damaged host cells releasing chemical signals key step is extravasation
50
chronic inflamation characteristics
results in persistent presence of foreign things, potentially because of permanent tissue damage causes: infection, splinters, implants, irritants, etc. sustain activation of the inflammatory pathway
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purpose of inflamation
more circulation of lymphatic system and dilation of BV increased flow of fluid and cells, allowing innate immune to get to the infection site faster pain receptor signaling its important to minimize usage of inflamed area
52
how do phagocytes recognize foreign cels
phagocytosis and opsonization (antibodies coating pathogen to facilitate phagocytoses, which is why encapsulated organisms are harder to phagocytose)
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what do phagocytes use to move toward and adhere to the pathogen
chemotaxis
54
what forms when phagocyte ingests pathogen and enclsoes it with a membrane bound vesicle
phagosome
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what does phagosome lysosome fusion form
phagolysosome
56
what does phagolysome permit
enzymes and toxic substances to come into contact with the pathogen and digest it
57
what types of substances do phagolysosome permit?
oxygen independent - lysosome, lactoferrin, defensis oxygen dependent - radicals, myeloperoxidase (produces HOCl) reactive nitrogen intermediates (nitric oxide, nitride ions, etc.)
58
What pathogen avoids phagocytosis by triggering apoptosis
shigella
59
what pathogen avoids consequences of phagocytosis by escaping
shigella and listeria
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what pathogen avoids consequences of phagocytosis by preventing the phagosome-lysosome fusion
salmonella
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what pathogen avoids the consequences of phagocytosis by living WITHIN the phagosome
coxiella: causes Q fever in humans, transmitted from animals (zoonosis), obligate intracellular pathogen, found in birth products (placenta, amniotic fluid, etc.)
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what are interferons
low mass cytokines produced by eukaryotic cells in response to intracellular infection
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Type I interferon
IFN alpha, beta, omega antiviral binds to receptors on uninfected host cells induce dsRNA endonuclease (prevents translation of viral RNA)
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Type II interferon
IFN gamma immunomodulatory mainly in adaptive immunity activates signal cascades in macrophages, NK cells, T cells increases MHC II on cell surfaces
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Natural Killer Cells function/target
find and destroy infected host cells and cancer cells target: MHC class 1 molecules, antibody Fc receptors (ADCC) if the host cell doesn't have MHC class 1 molecules, it is destroyed
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Toll like receptors (TLR) (innate)
protein receptors on a host cell membrane that can recognize MAMPs when attached (outside the cell) They then send a signal to inside the cell to produce interferons and release cytokines out of the cell (for inflammation response)
67
how body ends inflammatory process
CD59 protein, which turns off the complement system (system meant to target foreign invaders but if left on too long, causes cell damage)
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complement
20 proteins in blood serum that prevents blood infections triggers cascade pathways
69
goal of complement cascade
insert pores into microbial membranes to destroy membrane integrity and kill the cell
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outcome of complement pathways
creates membrane attack complexes (MACs) which cause cytoplasmic leaks attracts WBC facilitates phagocytosis/opsonization
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3 types of complement activating pathways
classical - depends on antibody/adaptive immune system alternative - doesn't require immunity lectin - requires synthesis of mannose binding lectin in response to cytokine released from macrophage
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which is the fastest pathway? slowest?
alternative classical (slowest)
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classical steps
antibodies bind to antigens, activating C1 C1 splits and activates C2 and C4 C2a and C4b combine and activate C3
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alternative pathway steps
(pathogens that have never infected host) C3 present in blood combines with factors B,D, and P on microbe surface C3 splits into C3a and C3b, functioning the same as in the classical pathway
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C3
C3a - functions in inflammation C3b - functions in cytolysis and opsonization
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fever is anything above __
100.4 F
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Fever thermoregulators
heat sensors (spinal cord, skin, large organs) hypothalamus - thermostat that controls vasoconstriction/vasodilation
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vasoconstriction/vasodilation for fever
constriction: tightening of BV when cold vasodilation: relaxation of BV to release heat
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external pyrogens examples
bacterial toxins, activate the thermoregulatory center in hypothalamus (cytokines cause hypothalamus to release prostaglandins that reset the body's thermostat to higher temp) turning up the thermostat
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internal pyrogens
interferons, cytokines
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advantage/disadvantage of fever
good - enhanced immune response, reduce iron available to bacteria bad - uncomfortable for patient, too high of a fever (107.6+) damages brain
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lectin pathway
macrophages injest pathogens, releases cytokines that stimulate lectin production in liver MBL - binds to mannose, activates C2 and C4 C2a and C4b activate C3, which functions the same
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complement activation regulators
CD59 protein - no pore in membrane is formed protein factor H - prevents unncessary activation of the complement system c-reactive protein - activates complement after being turned on by cytokines
84
what substance resets the hypothalamic thermostat to a higher temperature
prostaglandins
85
antigen presenting cells (APC)
macrophages and dentritic
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defensins are positively charged molecules that kill microbes by
destroying the cytoplasmic membrane
87
What do natural killer cells use to target infected cells
perforin
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Lysozyme affects which feature of bacteria?
cell walls
89
vasoactive factors can do what?
widen blood vessels increase vascular permeability stimulate local nerve endings
90
which leukocyte is least abundant in blood
basophils
91
what is the main function of interferons in the immune response
to inhibit viral replication
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which cells primarily produce interferon - gamma
T cells and NK cells
93
How does the hypothalamus respond to pyrogens
by raising the body's thermostat