Test 3 Flashcards
0
Q
how do lymphatics function in lipid absorption
A
chyle in the lacteals
1
Q
what are the functions of the lymph system?
A
fluid recovery, lipid absorption, immunity
2
Q
the ability to fight off an infection, antigen, or organism
A
resistance
3
Q
a disease causing agent/organism
A
pathogen
4
Q
what are some examples of pathogens?
A
bacteria, virus, fungus, protists
5
Q
low ability to fight off an infection
A
susceptibility
6
Q
what are the two types of resistance mechanisms?
A
non-specific resistance and specific resistance
7
Q
what are the characteristics of non-specific defense mechanisms?
A
not particular about what it is defending against, same mechanisms against all invaders, innate immunity, little specificity
8
Q
innate immunity
A
immunity you were born with
9
Q
what are characteristics of specific resistance mechanisms?
A
high degree of specificity, must be acquired after birth, so specific that it only gives protection against certain strains
10
Q
what are the parts of non-specific resistance?
A
natural barriers, body secretions, chemicals, white blood cells, and body processes, and inflammation
11
Q
what are natural barriers of the immune system?
A
skin and serous membranes
12
Q
how does the skin provide a natural barrier?
A
the pathogen has to get through a lot of layers that can be easily sloughed off in order to get to the dermis where the live parts of the skin are
13
Q
how do serous membranes provide a natural barrier?
A
they line open cavities like the GI, reproductive, and respiratory tracts and secrete mucous. Pathogens get trapped in the mucous and are swallowed with it, go to the stomach were stomach acid neutralize them
14
Q
what are body secretions that help with non-specific immunity?
A
sebum, saliva, sweat/perspiration, bile, urine, vaginal fluid, gastric juices
15
Q
how does sebum help with immunity
A
contain antimicrobial and anti-fungal secretions
16
Q
saliva’s role in n.s. immunity
A
contains enzymes that destroy pathogens
17
Q
sweat’s role in n.s. immunity
A
contains chemicals that are bactericidal
18
Q
what is a bactericidal chemical in sweat?
A
dermicidin - found in skin and sweat
19
Q
what is B.O.?
A
rotting organisms on the skin that result from the chemical reaction with sweat that kills the organism
20
Q
how do urine, bile, vaginal fluids, and gastric juices aid in n.s. immunity?
A
they have low pH outside of most bacteria’s ranges
21
Q
what are chemicals that aid in n.s. immunity
A
compliment proteins, interferons, iron-binding protein, anti-microbial proteins, chemotaxicators
22
Q
how do chemical aspects of non-specific resistance typically work?
A
they separate out of fluids and eliminate agents
23
Q
what are compliment proteins
A
group of 30 or so proteins in plasma or membrane that were produced by the liver. cause a cascade/series of events that end with an agent being marked for destruction
24
are compliment proteins active when they are produced?
usually inactive when they are produced then a trigger activates these proteins
25
how are compliment proteins named when they are produced vs when they are activated?
when they are produced, they are named with a letter and a number. when they are activated, they are named with a letter, a number, and another lower case letter
26
the series of events that compliment proteins undergo that end with a pathogen being marked for destruction is called
compliment cascade
27
what are the ways that a compliment protein can be activated?
through classical pathways or through alternate and lectin pathways
28
pathway of activating compliment proteins that requires antibodies to become active, specific resistance mechanism
classical pathway
29
pathway that activates compliment proteins within which no antibodies are needed - non-specific defense
alternate pathways and lectin pathways
30
how do compliment proteins mark a pathogen for destruction?
phagocytosis enhancement, inflammation, immune clearance, cytolysis
31
what compliment protein acts in phagocytosis enhancement?
c3b
32
what does phagocytosis enhancement do?
makes it easier for the macrophages to get ahold of the organism
33
what is obsinization and what does it have to do with?
it is coating an organism so that it is easier to phagocytize. it has to do with phagocytosis enhancement
34
which compliment protein has to do with inflammation
c3a
35
how does inflammation aid in the immune response?
helps make capillaries more permeable so that cells can move into the tissues when they are needed
36
what is immune clearance?
a complex binds to RBCs that are not functioning so that they can be removed as they go through the spleen
37
what is cytolysis?
bursting/splitting of a cell
38
what compliment proteins help with cytolysis and what do they do?
c5b, c6, c7, c8, c9 form a membrane attack complex that binds to a pathogen and causes it to rupture
39
group of proteins that are produced by our cells, usually in response to a viral infection that alert neighboring cells of the viruses infection and prevents the spread of the virus
interferons
40
how do iron-binding proteins work?
hemoglobin has 4 subunits that bind 4 iron atoms, pathogens require iron. iron binding proteins prevent pathogens from using iron
41
what are some iron binding proteins, where are they produced and how do they work?
transferrin and ferretin are produced by the liver and they tie up iron so it can't be used, lactoferrin is found in breast-milk, it gives an infant protection
42
what are anti-microbial proteins?
small chains of amino acids that are produced locally within the area of an infection in small amounds
43
antimicrobial protein that is produced at the site of an injury
thrombocytins
44
antimicrobial protein that is produced by leukocytes at the area of an infection
cathelicidins and defensins
45
antimicrobial proteins that are produced at the skins surface and are enhanced by vitamin D
dermicidin
46
chemical that attracts macrophages and other leukocytes into an area when there is damage or infection
chemotaxicators
47
aggressive phagocyte that produces a respiratory burst
neutrophil
48
respiratory burst
after the neutrophil detects a pathogen, lysosomes filled with digestive enzymes move to the surface of the cell (granules), they rupture and the enzymes are released in degranulation
49
what common household chemical can neutrophils produce and how?
they can produce peroxide and hypochloride - bleach
| they are absorbing oxygen which turns into a super oxide anion which turns into bleach
50
leukocyte associated with mucous membranes that secretes antihistamines which help to dampen an allergic respons
eosinophils
51
present in allergic responses and parasitic worm infections
eosinophils
52
what types of things will eosinophils form?
they will form peroxide, toxins, and antihistamines
53
why and when will an eosinophil form toxins?
they form toxins in parasitic worm infections because parasitic worms are animals
54
basophils
leukocyte that helps other leukocytes by secreting histamine, leukotriennes, and heparin
55
creates cellular swelling that allow leukocytes to move into infected cells
histamines
56
attract neutrophils and eosinophils
leukotriennes
57
reduces blood clotting - keeps blood flowing so that leukocytes can move into an area
haparin
58
what are the 3 types of lymphocytes?
natural killer cells, t lymphocytes, and b lymphocytes
59
search and destroy assassins that circulate in the blood and kill pathogens
natural killer cells
60
chemicals that poke holes in the membrane of the pathogen
perforins
61
how do natural killer cells function in immune surveillance?
they bind to the pathogen and release perforins and granzymes
62
what are granzymes
protein degrading enzymes
63
leukocyte that is aggressively phagocytic and emigrates from the blood stream to the tissues
monocytes
64
what are body processes for non-specific resistance?
fever and phagocytosis
65
how does a fever work?
it is a temporary reset of the body's hypothalamus thermostat. Raises the temperature 2-5 degrees.
66
pyrexia
fever
67
febrile
have a fever
68
antipyretic
chemical that reduces a fever
69
what are the benefits of a fever and are they large?
small benefits for a small amount of time. they decrease the activity of enzymes in pathogens by decreasing their growth, they promote interferon activity, and they increase metabolism which promotes healing
70
prostoglandins
cause fever and pain
71
how does an antipyretic work?
it inhibits prostaglandins
72
how does a pathogen cause fever?
the pathogen enters the body and the hypothalamus responds by secreting prostaglandins which increase the raised thermostat
73
what are the three stages of a fever?
1. onset - body temperature starts to rise, arteries constrict, clammy hands, cool skin, chills
2. stadium - body temp stays around the new set point
3. defervescence - decline in body tem, back to normal, sweating, skin warm and flushed, starting to get rid of heat
74
process whereby particulate matter or cells are engulfed and brought into the cell
phagocytosis
75
what must phagocytic cells be able to do?
change their shape
76
what are phagocytic cells?
white blood cells and their derivatives - neutrophils, monocytes, macrophages are the most phagocytic
77
what are the steps to phagocytosis
chemotaxis, adherence, ingestion, digestion and killing, exocytosis
78
what happens during step 1 of phagocytosis - chemotaxis?
cells start to move towards a chemical signal that is being released by the pathogen an the damaged tissue. damage or infection has been caused by a pathogen in a tissue and this needs to be removed. selectins cause endothelial cells to get sticky so that leukocytes stick to the capillary walls, margination occurs, emigration/diapedisis, and then the leukocytes are extravasated. OVERALL EFFECT: LEUKOCYTES MOVE FROM THE BLOOD INTO THE TISSUE IN RESPONSE TO CHEMICAL SIGNALS
79
chemicals in the capillary that cause endothelial cells to get sticky
selectins
80
movement of leukocytes along the edge of a capillary - caused by selectins
margination
81
leukocytes exit the capillaries into the tissues by squeezing through clefts
emigration/diapedesis
82
leukocytes have left the blood stream and entered the tissue
extravasated
83
what occurs during the second step of phagocytosis - adherence
physically attach the phagocyte to the pathogen to pull it into the cell through mediation by surface receptors
84
what problems can occur during adherence
pathogens can have capsules that make it hard for the phagocytes to attach to them, so the immune system has a tough time dealing with them
85
what can be done if there are problems with adherance?
opsinization - hand holds are made on the cells surface so that the phagocyte can adhere to the pathogen
86
what occurs during step 3, ingestion, of phagocytosis
phagocyte extends its pseudopods towards and around the pathogen, once the pathogen is engulfed, the membrane fuses to form a vesicle around the pathogen
87
phagosome
a vesicle with the engulfed pathogen in it - problem is that the pathogen is still alive even though it is in the cell
88
what happens during step 4, digestion and killing, of phagocytosis?
lysosomes migrate to the phagosome, lysosome membrane fuses with the phagosome and digestive enzymes are released and attack the pathogen - the container is now called a phagolysosome
89
what happens during step 5, exocytosis, of phagocytosis?
the particulate matter that is left over from the pathogens breakdown is removed. it is now in a third container called a residual body. this moves to the edge of the phagocyte and the membrane fuses with the plama membrane. the waste is released outside of the cell
90
vesicle with degraded waste that needs to be eliminated during stage 5 of phagocytosis
residual body
91
when does inflammation usually occur?
in response to an injury or an infection
92
how does inflammation function in non-specific resistance?
need to keep pathogens from spreading or moving so that we can destroy them, need to remove wreckage of damaged tissue, in order to begin the repair process
93
what are the 4 cardinal signs of inflammation
edema, erythema, pain, localized fever, (sometimes a loss of function as well)
94
why does edema and erythema occur in inflammation?
due to increased blood flow to an area
95
erythema
redness
96
what are the three major processes in inflammation that help fight off invaders?
1. mobilization of the body's defenses
2. containment and destruction of the pathogen
3. clean-up and repair
97
increase in blood flow to an area
hyperemia
98
chemicals that dilate blood vessels
vasoactive chemicals
99
what vasoactive chemicals are used in mobilization of body defenses for inflammation
histamin, leukotriennes, cytokines, prostaglandins, and complement proteins
100
what occurs in mobilization of the body's defenses for inflammation?
there is an increase in vasodilation of arterioles and an increased permeability of capillaries
101
how does histamine affect inflammation and how is it produced?
produced by mast cells and basophils, causes vasodilation and increased capillary permeability - this causes albumins to leave the blood and water follows which causes edema
102
how do leukotriennes function in inflammation and what are they produced by
produced by basophils and mast cells. they cause vasodilation and increased capillary permeability, they are also chemotaxicators so they attract other leukocytes to the area
103
what is the difference between paracrine and autocrine?
paracrine acts on neighboring cells while autocrine acts on the cell that secreted the signal
104
group of small proteins that are part of the communication/chemical signaling between WBCs
cytokines
105
what are some cytokines?
interferons, interleukins, chemotactic factors, colony stimulating hormones
106
what are chemotactic factors
involved in attracting leukocytes - includes bradykinin which increases vasodilation, capillary permeability and attracts neutrophils, it is involved in stimulating pain receptors
107
what are prostaglandins and where are they found?
group of lipid hormones found in the membrane that enhance histamine, bradykinin, promote pain and fever, and are a chemotaxic agent because they promote emigration of leukocytes from the blood stream
108
what occurs during the containment and destruction phase of inflammation?
a clot is built around the base of the infection that walls it off to trap the pathogen inside with the leukocytes and antibodies
109
what are some proteins that help with the containment and destruction phase of inflammation and how?
fibrinogen is an inactive large protein that is normally found in plasma and is inactive in water, but thrombin truns it into fibrin which moves into the tissue and forms a netlike arrangement that forms a clot
heparin prevents the clot from forming until the leukocytes get to the area
110
what happens during the clean-up and repair stage of inflammation
monocytes emigrate from the bloodstream and become macrophages that engulf pathogens by phagocytosis, then they act as antigen presenting cells, goes into lymphatics, pyogenesis can occur
111
pyogenesis
puss formatoin
112
pus
dead or dying WBC, debris, fluid, dead pathogens/residual bodies
113
how is pus drained or removed from the body most often?
cough, urinary tract, digestive tract
114
what is it called when pus is reabsorbed
an abscess
115
is specific resistance innate?
no, it must be acquired
116
what types of antigens do you build specific immunity to?
only ones that you have encountered
117
why is specific immunity called adaptive immunity?
the body adapts based on pathogens encountered
118
anything that the body recognizes as being foreign and that triggers an immune response
antigen
119
antigenic determinant
part of the pathogen that is recognized as foreign
120
o antigen
cell wall
121
h antigen
flagella
122
k antigen
capsule
123
hematopoiesis
blood formation
124
where are sites for hematopoiesis in the fetus
embryonic yolk sac, fetal liver, fetal bone marrow, fetal spleen, fetal lymph nodes, fetal thymus gland, fetal gut
125
what are sites for hematopoeisis in the adult
in functional red bone marrow - the flat bones of the skull, bodies of the vertebrae, sternum, ribs, os coxae, clavicle, scapula, proximal epiphysis of humor and femur
126
group of tissues that can form blood
myeloid tissue
127
precursor cell for all blood cells - pleuripotent, hemopoatic stem cell found in myeloid tissue
hemocytoblast
128
what happens to most leukocytes when they are formed and what are these cells?
they enter the blood stream and circulate - neutrophils, monocytes, eosinophils, basophils
129
what percentage of lymphocytes circulate in the blood stream and what are these called?
10% - natural killer cells, they release perforins
130
what happens to the other 90% of lymphocytes that are not being circulated in the blood stream?
they 'go to college' before they are released in order to become immunocompetent. once they are 'educated' they move to they lymphatics, lymph nodes, and peyers patches
131
immunocompetence
the ability to distinguish self cells from other cells
132
where are the two sites that lymphocytes become mature, or get 'educated'?
the bursa (bone marrow) and the thymus gland
133
what do lymphocytes become if they mature in the bursa?
b lymphocytes
134
what do lymphoctyes become when they mature in the thymus gland
t lymphocytes
135
anibody-mediated immunity and humoral immunity. they produce antibodies and wait for a specific antigen to enter the blood stream and then they bind to it
B cell lymphocytes
136
cell mediated immunity, do not use antibodies, most aggressive, directly attack pathogens
T cell lymphocytes
137
in what types of immunity do the pathogens have to be presented to the immune system before a response can occur?
both antibody-mediated and cell-mediated immunity
138
what are antigen presenting cells?
special phagocytes that do normal phagocytosis except for the fact that they do exocytosis of the residual body in a lymph node where B cells and T cells are present
139
what are some examples of antigen presenting cells
macrophages, dendritic cells (langerhan's cells), monocytes
140
humoral, antibody mediated immunity
B cell immunity
141
what occurs during B cell immunity?
a macrophage phagocytizes a pathogen that has some antigenic portion, the antigen is presented to a B cell in the lymph node which recognizes certain antigens it was trained to recognize. that B cell becomes activated because they bind to this antigen, it becomes very large and undergoes thousands of mitotic divisions so there are now thousands of activated B cels that recognize that fragment
142
clonal selection
B cell that has recognized an antigen undergoes many mitotic divisions to get 1000s of cells that also recognize that antigen
143
what are the 2 subpopulations that are produced following clonal selection of a B cell
plasma cells and memory cells
144
these cells make reaction time shorter on the next exposure to an antigen, they become inactive directly after production and are stored for later use where they will respond if their antigen is present
memory cells
145
effector cells that become very specialized. produce specific antibodies to destroy a pathogen
plasma cells
146
what are ways to eliminate antigens?
opsinization, agglutination, neutralization, cytolysis
147
antibodies clump bacteria together
agglutination
148
neutralizes a toxin
neutralization
149
helps with lysing a cell
cytolysis
150
what part of an antibodies structure is the same for all antibodies in a specific class?
the heavy chain
151
which parts of an antibody provide the variable region that provides specificity and varies between antibodies
light chain
152
part of an antibody that gives it its flexibility for binding
hinge
153
what are the classes of antibodies?
IgG, IgA, IgM, IgD, IgE
154
most abundant class of antibody, effective against bacteria, toxins, viruses, protists, can cross placenta between mother and fetus via transcytosis
IgG
155
how much of the circulating antibodies does IgG make up?
80-85%
156
secretory antibodies that are found in secretions like tears, saliva, sweat, vaginal fluid, milk, etc. have a dimer
IgA
157
secretory piece on an antibody
dimer
158
what percent of circulating antibodies does IgA make up?
10-15%
159
what percent of circulating antibodies does IgM make up?
5-10%
160
first antibody produced in the primary immune response, important in triggering agglutination, pentamer so that it can bind to a lot of antigens at once and clump them together
IgM
161
primary immune response
the first time you encounter an antigen, takes time to eliminate the pathogen and there is enough time for you to get sick, but you do eventually eliminate the pathogen
162
secondary antibody response
subsequent exposure to an antigen, have no symptoms, or they are more mild
163
fairly rare antibody usually found in the plasma membrane of B cells that serves as a receptor involved in the attachment of the B cell to the antigen before clonal selection, monomer
IgD
164
what is the percentage of IgD
about .2%
165
rare antibody in the membrane of mast cells and basophils. Associated with allergic reactions and parasitic worm infections
IgE
166
what is the percentage of circulating IgE
~.1%
167
what happens during a cell mediated response?
an antigen is phagocytized by a macrophage. In the lymph node, the antigen is presented to a colony/group of T cells and B cells - if they have the right receptors they will recognize the antigen and enlarge - goes through clonal selection and get millions of cells that recognize the antigen
168
what subpopulations of T cells are produced
memory T cells, helper T cells, cytotoxic T cells
169
inactive T cells that become activated in the presence of a pathogen and trigger a response
memory T cells
170
T cells that become activated by binding to an antigen, they are important in the coordination of an immune response and necessary for both B cell and T cell lines, release chemicals to sound the alarm, maximize phagocytosis and macrophages, activates and encourages the growth of cytotoxic T cells, vital for all immune function
helper T cells
171
why are helper T cells vital for all immune functions?
links all immunity, help all other cells in the immune system
172
how does HIV work?
hacks helper T cells so immune system is crippled and doesnt have the normal lines of defense
173
effector T cells that hunt down pathogens and eliminate them they are very potent and migrate all over the body looking for chemical signals that let them know a pathogen is there
cytotoxic T cells (cd8)
174
what are two ways that cytotoxic T cells can eliminate a pathogen
directly or indirectly
175
how do cytotoxic T cells eliminate pathogens directly?
through granzymes, perforin, granulysin, lymphotoxin
176
how do granzymes directly eliminate a pathogen?
they bind to the target cell and cause it to explode so that the antibodies can now bind to it and do phagocytosis
177
how does granulysin directly eliminate a pathogen
it is a chemical that facilitates the insertion of perforin into a cell membrane
178
how does lymphotoxin directly eliminate a pathogen?
contains a DNA fragmenting enzyme that is inserted into the perforin tubes and destroys the cell
179
controls the release of lymphotoxin and protects healthy cells
suppressor T cell
180
how do cytotoxic T cells indirectly eliminate a pathogen?
they release chemicals that attract phagocytes, such as macrophages, to the area - chemicals are gama interferons and macrophage migration inhibition factor
181
chemotaxic agent for several phagocytic cells, makes phagocytes more aggressive
gama interferons
182
keeps macrophages, monocytes, and other phagocytic cells in the area
macrophage migration inhibition factor
183
phenomenon where the immune system attacks itself
autoimmunity
184
when does autoimmunity occur?
when a pathogen has markers/determinants that resemble parts of the body
185
organism that has some markers that resemble some of the proteins on our heart valves which can cause Rheumatic fever and cause permanent damage to the heart valves
S. pyogenes
186
autoimmune thyroid follicles
myasthenia gravis
187
occurs when the immune system attacks synovial membrane in joints and can cause small bones to fuse together
rheumatoid arthritis
188
what things can cause an autoimmune disorder
S. pyogenes, myasthenia gravis, some forms of diabetes, grave's disease, rheumatoid arthritis
189
what is typically used to treat an autoimmune disorder
immunosupressants - makes people more susceptible to pathogens, though
190
what are the main cells that respond when a transplant is rejected?
mostly killer T cells and some antibody responses
191
transplant taken from someone who is genetically identical to you
isograph
192
transplant taken from the same species with a different genetic background, who makes the best case scenario for this?
autograph, siblings are the best
193
how do they determine a match for a transplant?
cross match 24 different proteins, if 6 are in common it is considered a match
194
cross-species transplants
xenograph
195
transplant taken from yourself - best type
autograph
196
what are 3 ways to acquire immunity?
active immunity, passive immunity, artificially acquired immunity
197
immunity received from a natural encounter with a pathogen, you will have symptoms and recover - memory cells provide immunity. long-lasting because memory cells were created
active immunity or naturally acquired immunity
198
immunity you get when antibodies are pumped in you that you didn't produce, like when a newborn gets antibodies through mother's milk
passive immunity
199
immunity that you get when you purposefully inject a weakened antigen/pathogen into your body. get the benefit of immunity without having to have the disease, sometimes need a booster
artificially acquired immunity
