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Anatomy and Physiology 2 > Test 3 > Flashcards

Test 3 Flashcards

0
Q

how do lymphatics function in lipid absorption

A

chyle in the lacteals

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1
Q

what are the functions of the lymph system?

A

fluid recovery, lipid absorption, immunity

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2
Q

the ability to fight off an infection, antigen, or organism

A

resistance

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3
Q

a disease causing agent/organism

A

pathogen

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4
Q

what are some examples of pathogens?

A

bacteria, virus, fungus, protists

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5
Q

low ability to fight off an infection

A

susceptibility

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6
Q

what are the two types of resistance mechanisms?

A

non-specific resistance and specific resistance

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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

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8
Q

innate immunity

A

immunity you were born with

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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

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10
Q

what are the parts of non-specific resistance?

A

natural barriers, body secretions, chemicals, white blood cells, and body processes, and inflammation

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11
Q

what are natural barriers of the immune system?

A

skin and serous membranes

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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

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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

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14
Q

what are body secretions that help with non-specific immunity?

A

sebum, saliva, sweat/perspiration, bile, urine, vaginal fluid, gastric juices

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15
Q

how does sebum help with immunity

A

contain antimicrobial and anti-fungal secretions

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16
Q

saliva’s role in n.s. immunity

A

contains enzymes that destroy pathogens

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17
Q

sweat’s role in n.s. immunity

A

contains chemicals that are bactericidal

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18
Q

what is a bactericidal chemical in sweat?

A

dermicidin - found in skin and sweat

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19
Q

what is B.O.?

A

rotting organisms on the skin that result from the chemical reaction with sweat that kills the organism

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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

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21
Q

what are chemicals that aid in n.s. immunity

A

compliment proteins, interferons, iron-binding protein, anti-microbial proteins, chemotaxicators

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22
Q

how do chemical aspects of non-specific resistance typically work?

A

they separate out of fluids and eliminate agents

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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

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24
Q

are compliment proteins active when they are produced?

A

usually inactive when they are produced then a trigger activates these proteins

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25
Q

how are compliment proteins named when they are produced vs when they are activated?

A

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

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26
Q

the series of events that compliment proteins undergo that end with a pathogen being marked for destruction is called

A

compliment cascade

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27
Q

what are the ways that a compliment protein can be activated?

A

through classical pathways or through alternate and lectin pathways

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28
Q

pathway of activating compliment proteins that requires antibodies to become active, specific resistance mechanism

A

classical pathway

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29
Q

pathway that activates compliment proteins within which no antibodies are needed - non-specific defense

A

alternate pathways and lectin pathways

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30
Q

how do compliment proteins mark a pathogen for destruction?

A

phagocytosis enhancement, inflammation, immune clearance, cytolysis

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31
Q

what compliment protein acts in phagocytosis enhancement?

A

c3b

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32
Q

what does phagocytosis enhancement do?

A

makes it easier for the macrophages to get ahold of the organism

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33
Q

what is obsinization and what does it have to do with?

A

it is coating an organism so that it is easier to phagocytize. it has to do with phagocytosis enhancement

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34
Q

which compliment protein has to do with inflammation

A

c3a

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35
Q

how does inflammation aid in the immune response?

A

helps make capillaries more permeable so that cells can move into the tissues when they are needed

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36
Q

what is immune clearance?

A

a complex binds to RBCs that are not functioning so that they can be removed as they go through the spleen

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37
Q

what is cytolysis?

A

bursting/splitting of a cell

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38
Q

what compliment proteins help with cytolysis and what do they do?

A

c5b, c6, c7, c8, c9 form a membrane attack complex that binds to a pathogen and causes it to rupture

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39
Q

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

A

interferons

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40
Q

how do iron-binding proteins work?

A

hemoglobin has 4 subunits that bind 4 iron atoms, pathogens require iron. iron binding proteins prevent pathogens from using iron

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41
Q

what are some iron binding proteins, where are they produced and how do they work?

A

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

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42
Q

what are anti-microbial proteins?

A

small chains of amino acids that are produced locally within the area of an infection in small amounds

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43
Q

antimicrobial protein that is produced at the site of an injury

A

thrombocytins

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44
Q

antimicrobial protein that is produced by leukocytes at the area of an infection

A

cathelicidins and defensins

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45
Q

antimicrobial proteins that are produced at the skins surface and are enhanced by vitamin D

A

dermicidin

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46
Q

chemical that attracts macrophages and other leukocytes into an area when there is damage or infection

A

chemotaxicators

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47
Q

aggressive phagocyte that produces a respiratory burst

A

neutrophil

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48
Q

respiratory burst

A

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

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49
Q

what common household chemical can neutrophils produce and how?

A

they can produce peroxide and hypochloride - bleach

they are absorbing oxygen which turns into a super oxide anion which turns into bleach

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50
Q

leukocyte associated with mucous membranes that secretes antihistamines which help to dampen an allergic respons

A

eosinophils

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51
Q

present in allergic responses and parasitic worm infections

A

eosinophils

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52
Q

what types of things will eosinophils form?

A

they will form peroxide, toxins, and antihistamines

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53
Q

why and when will an eosinophil form toxins?

A

they form toxins in parasitic worm infections because parasitic worms are animals

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54
Q

basophils

A

leukocyte that helps other leukocytes by secreting histamine, leukotriennes, and heparin

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55
Q

creates cellular swelling that allow leukocytes to move into infected cells

A

histamines

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56
Q

attract neutrophils and eosinophils

A

leukotriennes

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57
Q

reduces blood clotting - keeps blood flowing so that leukocytes can move into an area

A

haparin

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58
Q

what are the 3 types of lymphocytes?

A

natural killer cells, t lymphocytes, and b lymphocytes

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59
Q

search and destroy assassins that circulate in the blood and kill pathogens

A

natural killer cells

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60
Q

chemicals that poke holes in the membrane of the pathogen

A

perforins

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61
Q

how do natural killer cells function in immune surveillance?

A

they bind to the pathogen and release perforins and granzymes

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62
Q

what are granzymes

A

protein degrading enzymes

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63
Q

leukocyte that is aggressively phagocytic and emigrates from the blood stream to the tissues

A

monocytes

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64
Q

what are body processes for non-specific resistance?

A

fever and phagocytosis

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65
Q

how does a fever work?

A

it is a temporary reset of the body’s hypothalamus thermostat. Raises the temperature 2-5 degrees.

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66
Q

pyrexia

A

fever

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67
Q

febrile

A

have a fever

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68
Q

antipyretic

A

chemical that reduces a fever

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69
Q

what are the benefits of a fever and are they large?

A

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

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70
Q

prostoglandins

A

cause fever and pain

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71
Q

how does an antipyretic work?

A

it inhibits prostaglandins

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72
Q

how does a pathogen cause fever?

A

the pathogen enters the body and the hypothalamus responds by secreting prostaglandins which increase the raised thermostat

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73
Q

what are the three stages of a fever?

A
  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
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74
Q

process whereby particulate matter or cells are engulfed and brought into the cell

A

phagocytosis

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75
Q

what must phagocytic cells be able to do?

A

change their shape

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76
Q

what are phagocytic cells?

A

white blood cells and their derivatives - neutrophils, monocytes, macrophages are the most phagocytic

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77
Q

what are the steps to phagocytosis

A

chemotaxis, adherence, ingestion, digestion and killing, exocytosis

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78
Q

what happens during step 1 of phagocytosis - chemotaxis?

A

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

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79
Q

chemicals in the capillary that cause endothelial cells to get sticky

A

selectins

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80
Q

movement of leukocytes along the edge of a capillary - caused by selectins

A

margination

81
Q

leukocytes exit the capillaries into the tissues by squeezing through clefts

A

emigration/diapedesis

82
Q

leukocytes have left the blood stream and entered the tissue

A

extravasated

83
Q

what occurs during the second step of phagocytosis - adherence

A

physically attach the phagocyte to the pathogen to pull it into the cell through mediation by surface receptors

84
Q

what problems can occur during adherence

A

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
Q

what can be done if there are problems with adherance?

A

opsinization - hand holds are made on the cells surface so that the phagocyte can adhere to the pathogen

86
Q

what occurs during step 3, ingestion, of phagocytosis

A

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
Q

phagosome

A

a vesicle with the engulfed pathogen in it - problem is that the pathogen is still alive even though it is in the cell

88
Q

what happens during step 4, digestion and killing, of phagocytosis?

A

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
Q

what happens during step 5, exocytosis, of phagocytosis?

A

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
Q

vesicle with degraded waste that needs to be eliminated during stage 5 of phagocytosis

A

residual body

91
Q

when does inflammation usually occur?

A

in response to an injury or an infection

92
Q

how does inflammation function in non-specific resistance?

A

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
Q

what are the 4 cardinal signs of inflammation

A

edema, erythema, pain, localized fever, (sometimes a loss of function as well)

94
Q

why does edema and erythema occur in inflammation?

A

due to increased blood flow to an area

95
Q

erythema

A

redness

96
Q

what are the three major processes in inflammation that help fight off invaders?

A
  1. mobilization of the body’s defenses
  2. containment and destruction of the pathogen
  3. clean-up and repair
97
Q

increase in blood flow to an area

A

hyperemia

98
Q

chemicals that dilate blood vessels

A

vasoactive chemicals

99
Q

what vasoactive chemicals are used in mobilization of body defenses for inflammation

A

histamin, leukotriennes, cytokines, prostaglandins, and complement proteins

100
Q

what occurs in mobilization of the body’s defenses for inflammation?

A

there is an increase in vasodilation of arterioles and an increased permeability of capillaries

101
Q

how does histamine affect inflammation and how is it produced?

A

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
Q

how do leukotriennes function in inflammation and what are they produced by

A

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
Q

what is the difference between paracrine and autocrine?

A

paracrine acts on neighboring cells while autocrine acts on the cell that secreted the signal

104
Q

group of small proteins that are part of the communication/chemical signaling between WBCs

A

cytokines

105
Q

what are some cytokines?

A

interferons, interleukins, chemotactic factors, colony stimulating hormones

106
Q

what are chemotactic factors

A

involved in attracting leukocytes - includes bradykinin which increases vasodilation, capillary permeability and attracts neutrophils, it is involved in stimulating pain receptors

107
Q

what are prostaglandins and where are they found?

A

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
Q

what occurs during the containment and destruction phase of inflammation?

A

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
Q

what are some proteins that help with the containment and destruction phase of inflammation and how?

A

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
Q

what happens during the clean-up and repair stage of inflammation

A

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
Q

pyogenesis

A

puss formatoin

112
Q

pus

A

dead or dying WBC, debris, fluid, dead pathogens/residual bodies

113
Q

how is pus drained or removed from the body most often?

A

cough, urinary tract, digestive tract

114
Q

what is it called when pus is reabsorbed

A

an abscess

115
Q

is specific resistance innate?

A

no, it must be acquired

116
Q

what types of antigens do you build specific immunity to?

A

only ones that you have encountered

117
Q

why is specific immunity called adaptive immunity?

A

the body adapts based on pathogens encountered

118
Q

anything that the body recognizes as being foreign and that triggers an immune response

A

antigen

119
Q

antigenic determinant

A

part of the pathogen that is recognized as foreign

120
Q

o antigen

A

cell wall

121
Q

h antigen

A

flagella

122
Q

k antigen

A

capsule

123
Q

hematopoiesis

A

blood formation

124
Q

where are sites for hematopoiesis in the fetus

A

embryonic yolk sac, fetal liver, fetal bone marrow, fetal spleen, fetal lymph nodes, fetal thymus gland, fetal gut

125
Q

what are sites for hematopoeisis in the adult

A

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
Q

group of tissues that can form blood

A

myeloid tissue

127
Q

precursor cell for all blood cells - pleuripotent, hemopoatic stem cell found in myeloid tissue

A

hemocytoblast

128
Q

what happens to most leukocytes when they are formed and what are these cells?

A

they enter the blood stream and circulate - neutrophils, monocytes, eosinophils, basophils

129
Q

what percentage of lymphocytes circulate in the blood stream and what are these called?

A

10% - natural killer cells, they release perforins

130
Q

what happens to the other 90% of lymphocytes that are not being circulated in the blood stream?

A

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
Q

immunocompetence

A

the ability to distinguish self cells from other cells

132
Q

where are the two sites that lymphocytes become mature, or get ‘educated’?

A

the bursa (bone marrow) and the thymus gland

133
Q

what do lymphocytes become if they mature in the bursa?

A

b lymphocytes

134
Q

what do lymphoctyes become when they mature in the thymus gland

A

t lymphocytes

135
Q

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

A

B cell lymphocytes

136
Q

cell mediated immunity, do not use antibodies, most aggressive, directly attack pathogens

A

T cell lymphocytes

137
Q

in what types of immunity do the pathogens have to be presented to the immune system before a response can occur?

A

both antibody-mediated and cell-mediated immunity

138
Q

what are antigen presenting cells?

A

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
Q

what are some examples of antigen presenting cells

A

macrophages, dendritic cells (langerhan’s cells), monocytes

140
Q

humoral, antibody mediated immunity

A

B cell immunity

141
Q

what occurs during B cell immunity?

A

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
Q

clonal selection

A

B cell that has recognized an antigen undergoes many mitotic divisions to get 1000s of cells that also recognize that antigen

143
Q

what are the 2 subpopulations that are produced following clonal selection of a B cell

A

plasma cells and memory cells

144
Q

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

A

memory cells

145
Q

effector cells that become very specialized. produce specific antibodies to destroy a pathogen

A

plasma cells

146
Q

what are ways to eliminate antigens?

A

opsinization, agglutination, neutralization, cytolysis

147
Q

antibodies clump bacteria together

A

agglutination

148
Q

neutralizes a toxin

A

neutralization

149
Q

helps with lysing a cell

A

cytolysis

150
Q

what part of an antibodies structure is the same for all antibodies in a specific class?

A

the heavy chain

151
Q

which parts of an antibody provide the variable region that provides specificity and varies between antibodies

A

light chain

152
Q

part of an antibody that gives it its flexibility for binding

A

hinge

153
Q

what are the classes of antibodies?

A

IgG, IgA, IgM, IgD, IgE

154
Q

most abundant class of antibody, effective against bacteria, toxins, viruses, protists, can cross placenta between mother and fetus via transcytosis

A

IgG

155
Q

how much of the circulating antibodies does IgG make up?

A

80-85%

156
Q

secretory antibodies that are found in secretions like tears, saliva, sweat, vaginal fluid, milk, etc. have a dimer

A

IgA

157
Q

secretory piece on an antibody

A

dimer

158
Q

what percent of circulating antibodies does IgA make up?

A

10-15%

159
Q

what percent of circulating antibodies does IgM make up?

A

5-10%

160
Q

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

A

IgM

161
Q

primary immune response

A

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
Q

secondary antibody response

A

subsequent exposure to an antigen, have no symptoms, or they are more mild

163
Q

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

A

IgD

164
Q

what is the percentage of IgD

A

about .2%

165
Q

rare antibody in the membrane of mast cells and basophils. Associated with allergic reactions and parasitic worm infections

A

IgE

166
Q

what is the percentage of circulating IgE

A

~.1%

167
Q

what happens during a cell mediated response?

A

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
Q

what subpopulations of T cells are produced

A

memory T cells, helper T cells, cytotoxic T cells

169
Q

inactive T cells that become activated in the presence of a pathogen and trigger a response

A

memory T cells

170
Q

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

A

helper T cells

171
Q

why are helper T cells vital for all immune functions?

A

links all immunity, help all other cells in the immune system

172
Q

how does HIV work?

A

hacks helper T cells so immune system is crippled and doesnt have the normal lines of defense

173
Q

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

A

cytotoxic T cells (cd8)

174
Q

what are two ways that cytotoxic T cells can eliminate a pathogen

A

directly or indirectly

175
Q

how do cytotoxic T cells eliminate pathogens directly?

A

through granzymes, perforin, granulysin, lymphotoxin

176
Q

how do granzymes directly eliminate a pathogen?

A

they bind to the target cell and cause it to explode so that the antibodies can now bind to it and do phagocytosis

177
Q

how does granulysin directly eliminate a pathogen

A

it is a chemical that facilitates the insertion of perforin into a cell membrane

178
Q

how does lymphotoxin directly eliminate a pathogen?

A

contains a DNA fragmenting enzyme that is inserted into the perforin tubes and destroys the cell

179
Q

controls the release of lymphotoxin and protects healthy cells

A

suppressor T cell

180
Q

how do cytotoxic T cells indirectly eliminate a pathogen?

A

they release chemicals that attract phagocytes, such as macrophages, to the area - chemicals are gama interferons and macrophage migration inhibition factor

181
Q

chemotaxic agent for several phagocytic cells, makes phagocytes more aggressive

A

gama interferons

182
Q

keeps macrophages, monocytes, and other phagocytic cells in the area

A

macrophage migration inhibition factor

183
Q

phenomenon where the immune system attacks itself

A

autoimmunity

184
Q

when does autoimmunity occur?

A

when a pathogen has markers/determinants that resemble parts of the body

185
Q

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

A

S. pyogenes

186
Q

autoimmune thyroid follicles

A

myasthenia gravis

187
Q

occurs when the immune system attacks synovial membrane in joints and can cause small bones to fuse together

A

rheumatoid arthritis

188
Q

what things can cause an autoimmune disorder

A

S. pyogenes, myasthenia gravis, some forms of diabetes, grave’s disease, rheumatoid arthritis

189
Q

what is typically used to treat an autoimmune disorder

A

immunosupressants - makes people more susceptible to pathogens, though

190
Q

what are the main cells that respond when a transplant is rejected?

A

mostly killer T cells and some antibody responses

191
Q

transplant taken from someone who is genetically identical to you

A

isograph

192
Q

transplant taken from the same species with a different genetic background, who makes the best case scenario for this?

A

autograph, siblings are the best

193
Q

how do they determine a match for a transplant?

A

cross match 24 different proteins, if 6 are in common it is considered a match

194
Q

cross-species transplants

A

xenograph

195
Q

transplant taken from yourself - best type

A

autograph

196
Q

what are 3 ways to acquire immunity?

A

active immunity, passive immunity, artificially acquired immunity

197
Q

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

A

active immunity or naturally acquired immunity

198
Q

immunity you get when antibodies are pumped in you that you didn’t produce, like when a newborn gets antibodies through mother’s milk

A

passive immunity

199
Q

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

A

artificially acquired immunity

Anatomy and Physiology 2 (1 decks)

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