Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bio 245 > 3A > Flashcards

3A Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are the two types of hemocytoblasts?

A

-Myeloid line
- Lymphoid line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a hemocytoblast?

A

-multipotent stem cell
- all cells start here

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the types of Blood parts in the Myeloid line?

A

-erythrocytes/ RBCs
- platelet cells
- granulocytes/ monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do erythrocytes form?

A

form in red bone marrow in erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do platelets form?

A

Fragments form in red bone marrow from megakaryocytes in thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the types of granulocytes and monocytes?

A
  • neutrophil
  • basophil
  • eosinophil
  • monocyte
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do granulocytes/ monocytes form?

A

through leukopoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What blood cells are part of the Lymphoid line?

A
  • B-lymphocytes
  • T-lymphocytes
  • Natural killer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do lymphocytes mature?

A

In red bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where do t-lymphocytes and pre-t-lymphocytes form?

A

-develop in the red bone marrow and then migrate to the thymus where they mature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are t-lymphocytes comparable to?

A

special forces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where do Natural Killer Cells form?

A
  • this special type of lymphocyte matures in the red bone marrow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are NK cells comparable to?

A

hit men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What part of immunity are natural killer cells?

A

innate immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is innate immunity?

A
  • immediate response to a wide array of substances?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the type of innate immunity?

A

1st defense
- physical and chemical barriers
2nd line of defense
- non -specific internal defense
- physiological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the components of the 1st line of defense?

A
  • physical and chemical barriers like skin, membranes, and secretions
  • surface barriers and their secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the first line of defense do?

A

prevents entry of pathogens into the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the second line of defense composed of?

A
  • non-specific target cells and compounds that fight pathogens that have entered the body
  • non-specific internal defense including cells and antimicrobial compounds
  • physiological responses such as inflammation or fever.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Is the microbe identified in the first or second line of defense/ innate immunity?

A

NO
- just a broad defense against the bacteria but it doesn’t know what bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is adaptive immunity?

A

a delayed response to specific antigens with memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is included in adaptive immunity

A

cell-mediated and humoral branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why is adaptive immunity important

A
  • it allows for a stronger secondary response due to memory cells produced against a specific antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What directs the cell-mediated branch of adaptive immunity?

A

t-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What directs the humoral branch of adaptive immunity?

A

-b-lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What do first line of defense physical barriers include and do?

A

-includes mucous membranes and skin that protect our outer body (skin) and inner body surfaces (mucous membrane) these both prevent pathogens from entering the body
- the normal flora is on some surfaces that have commensal microbiota that helps prevent invading pathogens
- secretions from mucous membranes trap microbes allowing time for antimicrobial actions
- secretions are acidic interfering with bacteria growth
- lysosomes defensins, and dermcidin are secreting by skin and mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where are normal flora found?

A

on skin with commensal microbiota

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does skin and mucous do?

A

prevents pathogens from entering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What do secretions do?

A

-trap microbes allowing for antimicrobial actions
- secrete lysosomes, defensins, dermcidin
- have an acidic ph to deter bacteria growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Do secretions kill bacteria?

A

No, just deter it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What cells form the second line of defense?

A
  • phagocytic cells
  • proinflammatory secreting cells
  • apoptosis-initiating cells
  • parasite-destroying cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What do phagocytic cells do?

A

engulf pathogens to destroy them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What do proinflammatory secreting cells do?

A

secrete histamine, heparin, eicosanoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are eicosanoids?

A

local hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is heparin?

A

an anticoagulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What do histamines do?

A

stimulate vasodilation and increase permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What do apoptosis-initiating cells do?

A

trigger apoptosis in tells through the release of perforin which initates response and granzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does perforin do?

A

-pokes holes in cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What does granzyme do?

A

self-destruct button

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do parasite destroying cells do?

A

secrete a variety of substances that attack the surface of multicellular paracytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What do parasite destroying cells do?

A
  • secrete a variety of substances that attack the surface of multicellular parasites
    -death by 1000 papercuts
    -eosinophils go in like vultures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is an example of a parasite destroying cells?

A

eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is an example of an apoptosis-initiation cell?

A

NK (t-lymphocyte)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are examples of proinflammatory secreting cells?

A

-basophils in circulation
-mast cells in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the second line of defense?

A

antimicrobial components, physiological responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is an interferon?

A

a class of cytokines that nonspecifically impede viral spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the components of the second line of defense?

A

Interferons like
-IFn alpha and beta
-IFN gamma
Complements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What do ifn alpha and beta do?

A
  • bind to neighboring cells and prevent their infection by triggering the synthesis of enzymes that destroy viral nucleic acids and inhibit the synthesis of viral nucleic acids and proteins
  • stimulate NK cells to destroy the virus-infected cells (basically call NK cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Where is IFN alpha and beta produced?

A

produced by virus infected cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does IFN gamma do?

A

-stimulates the macrophages to destroy virus-infected cells
-serves as backup and cleans cell debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a complement antimicrobial component?

A
  • a group of plasma proteins that play a role in eliminating immune complex, cytolysis of pathogen cells, and opsonization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the difference between classical pathways and alternative pathways?

A
  • alternative pathways do not require or involve antibodies and classical pathways do
53
Q

What is a classical pathway?

A

when the plasma proteins bind directly to the antibody

54
Q

What does the classical pathway do?

A

eliminates immune complexes

55
Q

How does the classical pathway work?

A

the complement (C) cross-links (connects) immune (antigen-antibody) complexes to the erythrocyte, which transports to the liver and spleen
(acts like velcro that helps collect immune complexes and bring them to liver and spleen)

56
Q

What does the alternative pathway do?

A
  • the plasma proteins that bind directly to pathogen
  • preforms cytolysis or opsonization
57
Q

How does opsonization work?

A
  • complement (C) binds to pathogen and acts as an opsonin
  • enhances phagocytosis by flagging cells and enhancing inflammation
    -enhances inflammation by activating mast cells and basophils attracting neutrophils and macrophages to site
58
Q

How does cytolysis work?

A

-complement proteins create membrane attack complexes to lyse cell
- big holes allow in water leading to lysis.

59
Q

What is inflammation?

A

an immediate, localized sequence of events that occurs in reaction to injury or immune stimulation

60
Q

How does inflammation occur?

A
  • pro-inflammatory compounds (histamine) is released by injured tissue, basophils, mast cells, and infectious organisms
  • vascular changes triggered including vasodilation, increased capillary permeability, and increased cell adhesion molecules that support diapedesis of leukocytes
    -(cams act as speed bumps in margination)
  • leukocytes are recruited by margination (bind to cams) and undergo diapedesis and chemotaxis
    -plasma proteins exit the capillary decreasing capillary osmotic pressure and associated reabsorption
  • increased fluid and associated materials/cells picked up by lymphatic capillaries and delivered to lymph nodes for cleansing
61
Q

What is chemotaxis?

A

following of chemical cues to the injury site

62
Q

What is diapedesis?

A

exit capillary through endothelia

63
Q

What is histamine?

A

a pro inflammatory compound

64
Q

What do injured tissues release?

A

histamine

65
Q

What is histamine released by?

A

-injured tissue,
-basophils
-mast cells
-infections organisms

66
Q

What vascular changes occur during inflammation?

A
  • vasodilation
    -increased capillary permeability
    -increased CAMS
67
Q

What is a fever?

A

increase in body temp equal to or higher than 1 degree celsius from normal (37)

68
Q

What are signs of inflammation?

A

-redness due to increased blood flow
- heat due to increased blood flow and metabolic activity
- swelling due to increased volume in interstitial fluid
- pain due to the stimulation of pain receptors in area (bc swelling pushes on them)

69
Q

What first stimulates a fever?

A

pyrogens from immune cells and or infectious agents that circulate in the blood and trigger the hypothalamus to increase body temp

70
Q

Hoe is a controlled fever beneficial?

A

-must be low grade
- inhibits bacterial and viral growth, promoting immune activity, accelerating tissue repair

71
Q

What are the phases of fevers?

A
  1. onset: temps begin to rise
  2. stadium: elevated temp maintained
    3: defervescence : temp returns to normal
72
Q

What are the grades of fevers?

A
  • low grade: 100-101
  • intermidiate:102
  • high grade: 103-104
  • dangerous: over 104
73
Q

What is an antigen?

A
  • a molecule normally a protein or polysaccharide that is recognizable to immune cells through one or more of its epitopes
74
Q

What is an epitope?

A

antigenic determinant

75
Q

What does a self-antigen do?

A

recognizes the body’s tissues as self, allowing healthy tissue to be ignored by body’s immune system so no immune response is triggered
- also called immunotolerance

76
Q

What does a foreign antigen do?

A
  • stimulates an immune response (immunogenicity) by binding to either an antibody and or t-cell receptor located on t-lymphocytes
77
Q

What is an antibody?

A
  • immunoglobulin
  • a protein produced y specialized immune cells capable of recognizing, and binding to one or more epitopes on an antigen
78
Q

What is a major histocompatibility complex?

A

-MHC
- a group of genes responsible for forming MHC molecules
- genetically deteremined so they are unique to each person

79
Q

What are the MHC groups?

A

Class one and two

80
Q

What do class one MHC’s do?

A

-display endogenous proteins located inside the cell membrane of all nucleated cells
- in healthy cells these are self-antigens which should be ignored by the immune system
- in an infected cell these include foreign antigens which stimulates an immune response
-healthy cells have self-antigens on MHC1
- infected cells have foreign antigens on MHC1

81
Q

What do class two MHCs do?

A
  • produced in antigen-presenting cells only
  • phagocytic
  • APCs display exogenous proteins that originated outside the cell on MHC class two molecules
  • these exogenous proteins (antigenic) come from processed phagocytic molecules engulfed by APCs
  • essential in t-lymphocyte activation
    -basically rallies all the troops, shows and tells antigens it finds, but doesn’t kill it (don’t shoot the messenger)
82
Q

How do proteins get displayed on MHC cells?

A

-MHC1 cells are found on all nucleated cells
- self-antigens displayed on MHC1 are ignored/tolerated by the immune system
- MCH1 molecules are synthesized in the rER
-Self-antigen (peptide fragments of the cell) randomly bind to MHC1
- MHCI/self-antigen complex displayed at the membrane signaling to the immune system “all is well” and cell is ignored
- Infectious agents (viral particles or other microbes) enter the cell and are digested into fragments
-MHC1 molecules and processed foreign antigens combine and are transported to the plasma membrane
- MHC1 molecules are synthesized in the rER
-Processed foreign antigens bind to MHC 1
- MHC1/self-antigen complex is displayed at the cell membrane signaling to the immune system that “I’m sick” resulting in the apoptosis of the infected cell
-Only APCs synthesize MHCII molecules
APCs phagocytize an exogenous antigen (from an engulfed pathogen)
- secretory vesicles containing MHCII complex forms
- the complex is embedded in the cell membrane and communicates to the immune system that “this is what we should be looking for

83
Q

What does the APC and MHCII complex say?

A

this is what we should be looking for

84
Q

What synthesizes MHCII molecules?

A

APCs

85
Q

What do self antigen-mhc1 complexes say before an infectious agent is ingested?

A

I’m ok

86
Q

What do self antigen-mhc1 complexes say after an infectious agent is ingested?

A

I’m sick

87
Q

How many t-cell receptors are on a single cell?

A

multiple, identical antigenic t-cell receptors on a single cell

88
Q

How are t-lymphocyte classes shown?

A

-specific cell docking proteins are associated with the t-lymphocytes
- each lymphocyte has a specific CD

89
Q

How do Helper t-lymphocytes work?

A
  • display CD4 along the t-cell receptor
  • foreign antigens are processed by APCs and displayed on MHC2
  • TCR had specific genetically determined antigen binding sites
  • Helper t-cells are activated with binding
90
Q

What is CD4 on?

A

only helper t0lymphocytes and interacting with MHC2

91
Q

What are the types of t-lymphocytes

A

helper t-lymphocytes
cytotoxic t-lymphocytes

92
Q

How do cytotoxic t-lymphocytes work?

A

-displays CD8 along the side
-endogenous antigens are displayed on MHC1 of all nucleated cells
- TCR has specific genetically determined antigen binding sites as well
CD8 interacts with MHC1
- CTC activated with binding

93
Q

What is CD8 associated with

A

-MHC1
-Cytotoxic T-cells

94
Q

What are the two types of adaptive immunity?

A
  • cell-mediated
    -humoral immunity
95
Q

What is cell mediated immunity directed by?

A

-t-lymphocytes

96
Q

What is cell-mediated immunity effective against?

A

antigens within the cell

97
Q

How do Cytotoxic t-lymphocytes help with cell-mediated adaptive immunity

A
  • become activated by binding to foreign Antigens displayed on the infected cell
  • effector response is to trigger apoptosis of the infected cell through the release of perforin and granzyme y activated cytotoxic t-lymphocytes
  • activated cytotoxic t-cells CD8 target infected/ unhealthy cells stimulating them to undergo apoptosis
98
Q

How do helper t-cells help with cell-mediated adaptive immunity?

A
  • activated helper t-lymphocytes stimulate the proliferation of activated t-lymphocytes (cytotoxic and helper) and lymphocytes through the release of interleukins (IL2 + IL4)
  • basically helps humoral and cell mediated
99
Q

What is humoral immunity directed by?

A

b-lymphocytes

100
Q

What is humoral immunity effective against?

A

antigens outside of the cell

101
Q

How does humoral immunity work?

A
  • b-lymphocytes are activated when antigens bind to its b-cell receptors and the antigen BCR complex is engulfed, processed, and displayed
  • helper t-lymphocytes interact with this complex stimulating the proliferation of activated lymphocytes resulting in the formation of memory cells and plasma cells
  • effector response is the release of antibodies into the body fluids by newly produced plasma cells
  • activated b-cells release antibodies which act in a variety of ways to support the immune system
102
Q

What response does humoral immunity have?

A
  • the release of antibodies into the body fluids by newly produced plasma cells
  • activated B-cells release antibodies that act in a variety of ways to support the immune system
103
Q

How does co-stimulation of helper t-lymphocytes work?

A
  • during first stimulation CD4 on helper t-lymphocyte binds with MHC2 molecule on APC and TCR on helper t-lymphocytes interacts with antigen within the MHC2 molecule
    -during the second stimulation interleukin 2 (IL2) self-stimulates cloning of helper t-lymphocytes
  • this creates the effector response of activated t-lymphocytes releasing interleukin that acts to regulate immune cells
104
Q

How does the co-stimulation of B-lymphocytes work?

A

-1st stimulation the free antigen binds to BCR and B-lymphocyte engulfs (phagocytosis) complex and presents antigen to helper t-cell
- 2nd the stimulation the b cells act as an antigen-presenting cells and the helper t-lymphocytes bind to these cells and release IL-4 which triggers b-cell proliferation forming memory and plasma cells
-this has the effector response of antibodies being capable of recognizing the initial antigens and are secreted from plasma cells and circulating through the lymph and blood

105
Q

What happens when Antigens bond to the FAB site (f antigen binding site)

A
  • neutralization
    -aggulation
    =precipitation
106
Q

What is neutralization?

A

when the antibody binds to the fab site and covers the biologically active portion of the microbe or toxin
-binds to and blocks antigen to prevent it from becoming active
-

107
Q

What is aggulation?

A

when the antibody binds to the FAB site and cross-links cells like bacteria to form a clump

108
Q

What is precipitation?

A
  • when an antibody binds to the FAB site and cross-links circulating particles like toxins forming an insoluble antigen-antibody complex
  • particles are harder to identify when soluble so this makes them easier to identify
109
Q

What happens when a bacteria enters the body?

A

aggulation

110
Q

What is the F(C) site

A

constant region

111
Q

What happens when an antigen binds to the F(c) site

A

-complement fixation
- opsonization
- activation of NK cells

112
Q

What is complement fixation?

A

when an antibody binds to the FC region and complement proteins so that the complement is then activated

113
Q

What is opsonization

A

when the FC region of an antibody binds to receptors of phagocytic cells triggering and enhancing phagocytosis

114
Q

What is the activation of NK cells?

A
  • when the FC region of the antibody binds to an NK cell triggering the release of cytotoxic chemicals
  • antigens bind to antibodies, NK Cell binds to the constant region
115
Q

What is primary response?

A

the immunologic response to a first exposure

116
Q

What is a lag phase?

A

the initial period of no detectable antibodies

117
Q

What does exposure lead to in immunity?

A

the production of antibodies

118
Q

How soon does the production of antibodies happen?

A
  • within 1-2 weeks before antibodies peak and then it declines over time
119
Q

How does the production of antibodies start?

A

with plasma cells producing IGM and IGG

120
Q

What are the two types of acquired immunity?

A

passive and acive

121
Q

How is passive immunity acquired?

A
  • the transfer/ receiving of antibodies from another source
  • naturally acquired or artificially acquired
121
Q

How is natural passive immunity acquired?

A
  • transfer of maternal antibodies across the placenta or breast milk
  • short term protection
122
Q

How is artificial passive immunity acquired?

A
  • transfer of direct administration of collected antibodies
  • not quick or efficient
  • typically antitoxins or antivenoms
    -used when body doesn’t stand a chance of making it on its own
  • most people won’t ever need
122
Q

How is active immunity acquired?

A

-develops in response to antigen exposure
- we make antibodies

123
Q

How does naturally acquired active immunity happen?

A
  • develops after exposure to antigens in environment
124
Q

How does artificially acquired active immunity happen?

A
  • develops after administration of an antigen (usually through vaccination)
    -this stimulates an active immune response and promotes immunity to that particular antigen
125
Q

How do vaccines work?

A

vaccines stimulate the first exposure to build memory cells so the first real exposure looks like the second exposure would

126
Q

What is the difference between first and second exposure?

A
  • in first exposure igm is produced first than igg and the levels slowly rise
  • in second exposure antibody levels rise rapidly to a higher titer and last longer, predominantly igg, igg is now produced at the same time as IGM

Bio 245 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions