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A&P 2 > Lesson 12 > Flashcards

Lesson 12 Flashcards

1
Q

pathogens

A

agents capable of producing disease

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2
Q

pathogens include

A
  • viruses
  • bacteria
  • fungi
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3
Q

first line of defense against pathogens

A

skin and mucous membranes which serve as barriers

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4
Q

second line of defense

A

protections against pathogens that break the skin, mucous membrane barriers

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5
Q

what is included in the second line of defense?

A
  • leukocytes
  • macrophages
  • antimicrobial proteins
  • natural killer cells
  • fever
  • inflammation
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6
Q

third line of defense

A

adaptive immunity, mechanisms that defeat a specific pathogen and leave the body with a memory of it

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7
Q

immune system

A

widely distributed population of cells diverse chemical, physical barriers, and physiological responses

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8
Q

what are the two types of immune defenses?

A
  • innate
  • adaptive
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9
Q

innate immunity

A
  • defenses we are born with
  • protect us from broad spectrum of disease agents
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10
Q

innate immunity has a ___ effect

A

local

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11
Q

local effect of innate immunity

A

defends at point of invasion but there are exceptions

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12
Q

what in an exception to the local effect of innate immunity?

A

fever

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13
Q

innate immunity is _____

A

nonspecific

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14
Q

non-specificity of innate immunity

A

defenses are against a broad spectrum of disease agents rather than one particular pathogen

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15
Q

innate immunity lacks ____

A

memory

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16
Q

memory lacking in innate immunity

A

does not remember exposure to a specific pathogen

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17
Q

adaptive immunity

A

defenses against specific pathogens developed only upon exposure and maintain immune memory

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18
Q

protective features of the skin

A
  • toughness of keratin, difficult to penetrate
  • too dry and nutrient-poor to support much microbial growth
  • acid mantle
  • peptides that kill microbes present
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19
Q

what happens to microbes that are adhered to the skin

A

skin is continually shed with dead keratinocytes of the stratum corneum of the epithelium

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20
Q

acid mantle

A

thin filament of lactic and fatty acids from sweat and sebum that inhibits bacterial growth

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21
Q

what peptides are present in the skin that kill microbes

A
  • dermcidin
  • defensins
  • cathelicidins
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22
Q

what protects all tracts open to the exterior

A

mucous membranes

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23
Q

protective features of mucous membranes

A
  • sticky mucus physically traps microbes
  • presence of lysozyme
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24
Q

lysozyme

A

enzyme that destroys bacterial cell walls

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25
Q

____ is in skin and mucous membranes

A

subepithelial areolar tissue

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26
Q

subepithelial areolar tissue of skin and mucous membranes contain

A

viscous barrier of hyaluronic acid in ground substance

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27
Q

hyaluronic acid

A

large glycosaminoglycan

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28
Q

pathogens can release

A

hyaluronidase

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29
Q

hyaluronidase

A

enzyme to make hyaluronic acid less viscous

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30
Q

what is waiting when skin and mucous membranes are penetrated?

A
  • phagocytes
  • leukocytes
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31
Q

what are the five types of leukocytes?

A
  • neutrophils
  • eosinophils
  • basophile
  • monocytes
  • lymphocytes
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32
Q

neutrophils

A
  • wander in connective tissue
  • function to kill bacteria
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33
Q

neutrophils can ensnare bacteria by releasing

A

neutrophil extracellular trap

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34
Q

neutrophil extracellular trap (NET)

A

web of nuclear chromatin and proteins

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35
Q

how can neutrophils kill

A

phagocytizing and digesting microbe or by releasing bactericidal chemicals to create killing zone around neutrophil

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36
Q

eosinophils found especially in

A

mucous membrane

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37
Q

eosinophils guard against

A

large parasites like tapeworms and roundworms

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38
Q

eosinophil participate in

A

inflammation and allergic reactions

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39
Q

basophils secrete chemicals that do what?

A

aid mobility and action of other leukocytes

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40
Q

leukotrienes

A
  • vasodilator
  • increases blood flow and speeds delivery of leukocytes to the area
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41
Q

heparin

A

inhibits clot formation that would impede leukocyte mobility

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42
Q

mast cells

A

secrete histamine and heparin like basophils but in connective tissues

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43
Q

lymphocytes include

A
  • B cells
  • T cells
  • NK cells
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44
Q

T cells and B cells are apart of ___ immunity

A

adaptive

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45
Q

NK cells participate in ____ immunity

A

innate

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46
Q

monocytes

A

emigrate from blood into connective tissues and transform into macrophages

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47
Q

macrophage system

A

all the body’s avidly phagocytic cells except leukocytes

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48
Q

what is included in the macrophgae system

A
  • monocytes
  • macrophages
  • dendritic cells
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49
Q

some macrophages are ____ while others are _____

A
  • wandering
  • fixed
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50
Q

examples of specialized forms of macrophages in specific locations (3)

A
  • microglia (CNS)
  • alveolar macrophages (lungs)
  • stellate macrophages (liver)
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51
Q

blood-borne antimicrobial proteins

A
  • interferons
  • complement system
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52
Q

interferons

A

proteins secreted by virally infected cells and immune cells

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53
Q

interferons serve as

A

alarm to nearby cells

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54
Q

interferons bind to receptors on nearby cells and do what?

A

stim their synthesis of defensive antiviral proteins to prevent their infection

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55
Q

interferons activate ____ to do what?

A
  • NK cells and macrophages
  • better destroy infected cells or cancer cells
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56
Q

complement system

A

group of 30 or more globular proteins that contribute to both innate immunity and adaptive immunity

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57
Q

complement system synthesized mainly by

A

liver

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58
Q

complement system circulate in the blood in ___ form

A

inactive

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59
Q

what do activated complements participate in?

A
  • inflammation (C3a)
  • immune clearance (C3b)
  • phagocytosis (C3b)
  • cytosis (C3b)
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60
Q

three pathways of complement system activation

A
  • classical pathway
  • alternative pathway
  • lectin pathway
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61
Q

classical complement activation pathway is ___ than alternative pathway

A

faster

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62
Q

classical complement activation pathway requires

A

antibody binding to microbe

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63
Q

what happens in the classical pathway when the antibody binds to the microbe?

A

changes the antibody shape and exposes complement-binding sites on the antibody

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64
Q

binding of the ____ to the antibody sets off reaction cascade

A

complement C1

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65
Q

complement fixation

A

complement C1 binding on the antibody that sets off a reaction cascade

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66
Q

alternative complement activation pathway

A

complement C3b binds to microbe surface activating reaction cascade

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67
Q

lectins

A

plasma proteins that bind to carbohydrates on the pathogen’s surface activating reaction cascade

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68
Q

lectin complement activation cascade is dependent on

A

lectins

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69
Q

four outcomes of complement activation

A
  • inflammation
  • immune clearance
  • phagocytosis
  • cytolysis
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70
Q

inflammation as an outcome of complement activation

A

C3a stims mast cells and basophils to secrete histamine and other inflammatory chem which activate and attracts neutrophils and macrophages

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71
Q

immune clearance as an outcome of complement activation

A

C3b binds the antigen-antibody complexes to red blood cells that then circulate to the liver and spleen where macrophages strip off and destroy the Ag-Ab complexes leaving RBC unharmed

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72
Q

phagocytosis as an outcome of complement activation

A

C3b coats microbial cells and serves as binding sites for phagocyte attachment

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73
Q

what is it called when the microbial cell gets coated by C3b in phagocytosis after complement activation?

A

opsonization

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74
Q

cytolysis as an outcome of complement activation

A
  • complement C3b initiates formation C5b
  • C5b aggregates with other complement proteins within plasma membrane of microbe which forms the membrane attack complex
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75
Q

membrane attack complex

A

a hole in the target cell membrane

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76
Q

what does the membrane attack complex do

A
  • electrolytes leak out
  • water flows in rapidly
  • target cell ruptures
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77
Q

natural killer cells continually

A

patrol body looking for pathogens and diseased host cells

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78
Q

immunological surveillance

A

continually being on patrol for pathogens and diseased cells

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79
Q

what do NK cells do?

A

attack and destroy microbes, transplanted cells, cells infected with viruses, and cancer cells

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80
Q

how do NK cells destroy microbes

A

recognize infected cell and bind to it and release perforins

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81
Q

perforins

A

polymerize to form a ring to create a hole in the target’s plasma membrane

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82
Q

granzymes

A

group of protein-degrading enzymes

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83
Q

granzymes function

A

enter through pore and degrade intracellular enzymes and induce apoptosis

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84
Q

apoptosis

A

programmed cells death

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85
Q

cancer cells exhibit

A

tumor specific antigens

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86
Q

where are tumor-specific antigens located?

A

cell’s plasma membrane

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87
Q

cancer cells are identified as abnormal by

A

NK cells

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88
Q

immunological escape

A

cancer cells that destroy NK cells that detect them or avoid detection by not displaying tumor-specific antigens or masking them

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89
Q

in viral infections cells infected with virus present

A

abnormal proteins on their plasma membrane which allows NK cells to identify and destroy them

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90
Q

fever aka

A

pyrexia

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91
Q

fever

A

abnormal elevation of body temp

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92
Q

fever results from

A
  • trauma
  • infections
  • drug reactions
  • brain tumors
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93
Q

what does a fever do? (3)

A
  • promote interferon activity
  • elevates metabolic rate and accelerates tissue repair
  • inhibits reproduction of bacteria and viruses
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94
Q

recovery from fever is faster when

A

you let the fever take its course

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95
Q

antipyretics

A

fever reducing medications

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96
Q

stages of fever (3)

A
  • onset
  • stadium
  • defervescence
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97
Q

what the six steps of the course of a fever?

A
  • infection and pyrogen secretion
  • hypothalamic thermostat is reset to higher set point
  • onset
  • stadium
  • infection ends, set point returns to normal
  • defervescence
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98
Q

onset of fever

A

body temp rises

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99
Q

stadium of fever

A

body temp oscillates around set point

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100
Q

defervescence of fever

A

body temp returns to normal

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101
Q

reye syndrome

A

serious disorder in children younger than 15 following an acute viral infection such as chickenpox or flu

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102
Q

what can trigger reye syndrome

A

use of aspirin to control fever

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103
Q

what happens in reye syndrome

A
  • swelling of brain neurons
  • pressure of swelling brain
  • fatty infiltration of liver and other viscera
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104
Q

what are the symptoms of pressure of swelling brain (5)

A
  • nausea
  • vomiting
  • disorientation
  • seizures
  • coma
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105
Q

____ die of reye syndrome

A

30%

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106
Q

what happens to most survivors of reye syndrome

A

suffer intellectual disabilities

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107
Q

inflammation

A

local defensive response to tissue injury, trauma, or injury

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108
Q

general purposes of inflammation

A
  • limit spread of pathogens and destroy them
  • remove debris from damaged tissue and initiate tissue repair
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109
Q

four cardinal symptoms/signs of inflammation

A
  • redness
  • swelling
  • heat
  • pain
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110
Q

inflammation involves numerous

A

cytokines

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111
Q

cytokines

A

small proteins that function in chemical communication between cells

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112
Q

cytokines do what during inflammation

A

alter physiology of receiving cell

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113
Q

cytokines include

A
  • interferon
  • interleukins
  • tumor necrosis factor
  • chemotactic factors
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114
Q

most immediate requirement after tissue injury is

A

get defensive leukocytes to the site quickly

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115
Q

how are leukocytes moved to injury spot quickly?

A

local hyperemia

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116
Q

hyperemia

A

increased blood flow

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117
Q

what chemicals cause hyperemia?

A
  • histamine
  • leukotrienes
  • cytokines
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118
Q

what are vasodilators secreted by?

A
  • basophils
  • mast cells
  • cell damaged by trauma, toxins, or organisms triggering inflammation
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119
Q

hyperemia other function

A

washes toxins and metabolic waste from the site more rapidly

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120
Q

vasoactive chemicals stim

A

endothelial cells to contract

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121
Q

what happens when endothelial cells contract

A

widens gaps between them

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122
Q

what happens when gaps widen between endothelial cells?

A
  • increase capillary permeability
  • fluid, leukocytes, and plasma proteins leave bloodstream
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123
Q

cell adhesion molecules are made by

A

endothelial cells

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124
Q

what do cell adhesion molecules aid in

A

recruitment of leukocytes

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125
Q

how do cell adhesion molecules aid in recruitment of leukocytes

A

make membranes sticky so leukocytes adhere to vessel wall

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126
Q

margination

A

leukocytes adhering to vessel walls

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127
Q

diapedesis

A
  • emigration
  • leukocytes crawl through gaps in the endothelial cells and enter tissue fluid
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128
Q

extravasated

A

term for cells and chemicals that have left the bloodstream

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129
Q

what is the heat of inflammation caused by

A

hyperemia

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130
Q

what is the redness of inflammation caused by

A
  • hyperemia
  • extravasated RBCs in the tissue
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131
Q

what is swelling in inflammation caused by?

A

increased fluid filtration from the capillaries

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132
Q

what is pain in inflammation caused by?

A
  • direct injury to the nerves
  • pressure on the nerves from edema
  • stim of pain receptors by prostaglandins
  • bacterial toxins
  • bradykinin
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133
Q

other priority of inflammation

A

prevent pathogens from spreading throughout body

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134
Q

____ filters into tissue fluid and clots to form stick mesh that walls off microbes

A

fibrinogen

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135
Q

heparin prevents

A

clotting at site of injury

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136
Q

pathogens are in fluid pocket surrounded by

A

clot

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137
Q

pathogens are attacked by

A

antibodies, phagocytes, and other defenses

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138
Q

neutrophils accumulate at the injury site within

A

an hour

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139
Q

after leaving bloodstream neutrophils exhibit

A

chemotaxis

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140
Q

chemotaxis

A

attraction to chemicals that guide them to injury site

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141
Q

____ quickly respond to and kill bacteria

A

neutrophils

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142
Q

how do neutrophils kill bacteria

A

phagocytosis

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143
Q

respiratory burst

A

neutrophils absorb O2 to form H2O2 an release hypochlorite

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144
Q

hypochlorite

A

highly toxic and forms killing zone around cell

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145
Q

neutrophils secrete ____ for what function?

A
  • cytokines
  • recruitment of macrophages and additional neutrophils
146
Q

____ and ___ secrete colony-stimulating factor

A

macrophages and T cells

147
Q

what do colony-stimulating factors from macrophages and t cells do

A

stim leukopoiesis and raise WBC count

148
Q

neutrophilia

A

5000 cells/uL to 25000 cells/uL in bacterial infection

149
Q

eosinophilia

A

elevated eosinophil count in allergy or parasitic infection

150
Q

tissue cleanup and repair primarily involves

A

monocytes

151
Q

monocytes arrive in ____ and become macrophages

A

8-12 hours

152
Q

how do macrophages assist in tissue cleanup and repair

A

engulf and destroy bacteria, damages host cells, and dead and dying neutrophils

153
Q

____ contributes to tissue cleanup

A

edema

154
Q

how does edema contribute to tissue cleanup?

A

swelling compresses veins and reduces venous drainage

155
Q

forces of edema open valves of lymphatic capillaries, promoting

A

lymphatic drainage of bacteria, dead cells, and debris

156
Q

pus

A

yellow accumulation of dead neutrophils, bacteria, cellular debris, and tissue fluid

157
Q

abscess

A

accumulation of pus in a tissue cavity

158
Q

platelet-derived growth factor

A

secreted by blood platelets and endothelial cells in injured areas

159
Q

platelet-derived growth factor stims ___ to multiply and ____

A
  • fibroblasts
  • synthesize collagen
160
Q

hyperemia delivers oxygen, amino acids, and other necessities for ___

A

protein synthesis

161
Q

increased heat

A
  • increases metabolic rate
  • speeds mitosis
  • tissue repair
162
Q

_____ forms a scaffold for tissue reconstruction

A

fibrin clot

163
Q

pain does what for tissue repair

A

makes us limit the use of body part so it has chance to rest and heal

164
Q

_____ serves as the third line of defense

A

adaptive immunity

165
Q

what are the three characteristics that distinguish adaptive immunity and innate immunity?

A
  • systemic affect
  • specificity
  • memory
166
Q

systemic effect in adaptive immunity

A

acts throughout the body

167
Q

specificity in adaptive immunity

A

generates protection and immunity to specific pathogens on an individual basis

168
Q

memory in adaptive immunity

A
  • when re-exposed to the same pathogen
  • the body reacts so quickly that there is no noticeable illness
169
Q

two types of adaptive immunity

A
  • cellular
  • humoral
170
Q

what happens in cellular immunity

A

T lymphocytes directly attack and destroy foreign cells or diseased host cells

171
Q

cellular immunity aka

A

cell mediated

172
Q

what is the function of cellular immunity

A

rids the body of pathogens that reside in human cells where they are inaccessible to antibodies

173
Q

what does cellular immunity work against other than pathogens in cells?

A
  • parasitic worms
  • cancer cells
  • transplanted cells
174
Q

humoral immunity aka

A

antibody mediated

175
Q

what happens in humoral immunity

A

mediated by B cells that become plasma cells that release antibodies that do not directly destroy a pathogen but tag it for destruction

176
Q

humoral immunity is effective against

A
  • extracellular viruses
  • bacteria
  • yeasts
  • protozoans
  • molecular diseases agents
177
Q

what are molecular disease agents

A
  • toxins
  • venoms
  • allergens
178
Q

other forms of classifying immunity

A
  • natural active immunity
  • artificial active immunity
  • natural passive immunity
  • artificial passive immunity
179
Q

natural active immunity

A

production of one’s own antibodies or T cells as a result of infection or natural exposure to antigen

180
Q

example of natural active immunity

A

catching the flu and gaining immunity to that strain

181
Q

artificial active immunity

A

production of one’s own antibodies or T cells as a result of vaccination against disease

182
Q

vaccine

A

consists of dead or attenuated pathogens that stim the immune response without causing the disease

183
Q

booster shots

A

may be given to re-stim immune memory to maintain a high level of protection

184
Q

example of artificial active immunity

A

shots

185
Q

natural passive immunity

A

temporary immunity that results from antibodies produced by another person

186
Q

example of natural passive immunity (2)

A
  • fetus acquires antibodies from mother through placenta
  • baby acquires them during breast feeding
187
Q

artificial passive immunity

A

temporary immunity that results from the injection of immune serum from another person or animal

188
Q

immune serum

A

antibodies

189
Q

example of artificial passive immunity

A

emergency treatment for snakebite, botulism, tetanus, rabies, and other diseases

190
Q

antigen

A

any molecule that can bind an antibody

191
Q

most antigens have ___ MW

A

high

192
Q

what are antigens usually composed of?

A
  • proteins
  • polysaccharides
  • glycoproteins
  • glycolipids
193
Q

characteristics enable body to distinguish between

A

self and non self

194
Q

epitopes

A

certain regions of an antigen molecule that stim immune responses

195
Q

epitopes aka

A

antigenic determinants

196
Q

haptens

A

too small to be antigenic in themselves

197
Q

hapten aka

A

incomplete antigens

198
Q

haptens may trigger immune responses by

A

combining with a host molecule, creating a complex that the body recognizes as foreign

199
Q

examples of haptens

A
  • cosmetics
  • detergents
  • industrial chemical
  • poison ivy
  • animal dander
  • penicillin
200
Q

antibodies aka

A

immunoglobulins

201
Q

antibodies

A

defensive proteins that play a variety of defensive roles

202
Q

human immune system capable of ____ different antibodies

A

1 trillion

203
Q

soluble antibodies are dissolvable in what? (8)

A
  • blood plasma
  • tissue fluids
  • lymph
  • mucus
  • saliva
  • intestinal secretions
  • tears
  • breast milk
204
Q

antibody monomer

A

basic structural unit of an antibody

205
Q

antibody monomer composed of

A

four polypeptide chains linked by disulfide bonds

206
Q

what are the four polypeptide chains in antibody monomers called?

A

two heavy and two light chains

207
Q

all four polypeptide chains have ___ that give antibody its uniqueness

A

variable region

208
Q

antigen binding site formed from

A

the V regions of the heavy and light chain on each arm

209
Q

where does the antigen binding site attach

A

the epitope of an antigen molecule

210
Q

constant region has the ___ amino acid sequence as variable region

A

same

211
Q

what does the constant region determine

A

mechanism of antibody action

212
Q

antigen classes (5)

A
  • IgM
  • IgG
  • IgD
  • IgA
  • IgE
213
Q

IgA as monomer in

A

plasma

214
Q

IgA as dimer in

A
  • mucus
  • saliva
  • tears
  • breast milk
  • intestinal secretions
215
Q

IgA prevent

A

pathogen adherence to epithelia and penetrating underlying tissues

216
Q

IgA provides ____ immunity to newborns

A

passive

217
Q

IgD

A
  • monomer
  • B cell transmembrane antigen receptor
218
Q

IgD functions in

A

B cell activation by antigens

219
Q

IgE

A
  • monomer
  • bound to receptors on basophils and mast cells
220
Q

IgE stims what two things

A
  • release of histamine and other chemical mediators of inflammation and allergy
  • eosinophil defensive actions against parasites
221
Q

IgG

A
  • monomer
  • constitutes 80% of circulating antibodies
222
Q

IgG is the predominant antibody in ___

A

secondary immune response

223
Q

IgG is capable of

A
  • complement fixation
  • crossing placenta to fetus
224
Q

IgM

A

pentamer in plasma and lymph

225
Q

IgM is predominant antibody in ____

A

primary immune response

226
Q

IgM is capable of

A
  • strong agglutinating
  • complement fixing abilities
227
Q

three types of lymphocytes

A
  • NK cells
  • T cells
  • B cells
228
Q

NK cells are a part of ___ immunity

A

innate

229
Q

T and B cells are part of ___ immunity

A

adaptive

230
Q

T cell production

A

produced in red bone marrow but migrate to thymus to complete their maturation process

231
Q

positive selection

A

cortical epithelial cells test developing T cells to ensure they have the proper receptors

232
Q

what happens when positive selection does not occur

A

T cells die

233
Q

T cells can fail by

A

reacting to self antigen

234
Q

what happens to T cells that react to self antigen

A

they’re eliminated to ensure the immune system is self tolerant

235
Q

self tolerant

A

will not attack one’s own tissues

236
Q

anergy

A

self reactive T cells remain alive but unresponsive

237
Q

with proper receptors T cells become _____

A

immunocompetent

238
Q

immunocompetent

A

capable of recognizing antigens presented to them

239
Q

B cells development

A

develop entirely in red bone marrow

240
Q

what happens to B cells that react to self anitgens

A

undergo either anergy or clonal deletion

241
Q

self tolerant B cells do what?

A

synthesize antigen surface receptors, divide rapidly, produce immunocompetent clones

242
Q

B cells leave bone marrow and do what?

A

colonize lymphoid tissues and organs as T cells

243
Q

T cells can only recognize antigens presented by

A

antigen presenting cells

244
Q

APCs include

A

dendritic cells, macrophages, and B cells

245
Q

function of APCs depend on

A

MHC proteins

246
Q

MHC proteins are encoded by

A

major histocompatibility complex genes

247
Q

MHC proteins act as

A

cell identification tags

248
Q

cell identification tags

A

label every cell of your body as belonging to you

249
Q

what is the only instance that MHC proteins are not structurally unique

A

identical twins

250
Q

MHCs are displayed on ___ of APCs along with ___

A
  • surface
  • fragment of presented antigen
251
Q

antigen processing

A

APC encounters antigen, internalizes it by endocytosis, digests it into fragments, and attaches it to the MHC protein

252
Q

what happens after antigen processing

A

cell displays MHC protein with the antigen in its plasma membrane

253
Q

if APC displays a self antigen to a T cell

A

the T cell disregard it

254
Q

if an APC displays a non-self antigen to a T cells

A

the appropriate T cell will initiate an immune response against the source of that antigen

255
Q

APCs and lymphocytes communicate to cytokines called

A

interleukins

256
Q

cellular immunity

A

form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells

257
Q

classes of T cells

A
  • cytotoxic T cells
  • helper T cells
  • memory T cells
258
Q

cytotoxic T cells

A

carry out attack

259
Q

helper T cells

A

promote activities of other immune cells

260
Q

memory T cells

A

responsible for memory in cellular immunity

261
Q

what happens when APC encounters and processes an antigen

A

migrates to the hearest lymph node and displays it to the T cells

262
Q

when T cells encounter a displayed antigen on the MHC protein

A

they initiate an immune response

263
Q

what are the two classes of MHC T cells respond to

A
  • MHC-I
  • MHC-II
264
Q

MHC-I proteins

A
  • occur on all nucleated cells
  • internal peptides are presented on cell surface including virus-infected cells
  • cancer cells
265
Q

MH-II proteins

A
  • occur on APCs
  • external antigens are presented on cell surface
266
Q

cytotoxic T cells respond only to

A

MHC-I proteins

267
Q

helper T cells respond only to

A

MHC-II

268
Q

T cell activation begins when

A

Tc or Th cell binds to an MHC protein displaying an epitope that the T cell is programmed to recognize

269
Q

costimulation

A

additional signaling processes required for T cell activation

270
Q

in addition to MHC and antigen binding T cells must also bind

A

signaling proteins on surface of APCs in damaged/infected tissues

271
Q

what is the purpose of T cells binding to signaling proteins?

A

helps to ensure the immune system doesn’t launch an attack in the absence of an enemy

272
Q

what happens if T cells don’t bind to the signaling proteins

A

autoimmune disorders

273
Q

successful T cell activation will trigger

A

clonal selection

274
Q

activated T cell undergoes

A

repeated mitosis

275
Q

repeated mitosis of activated T cells gives rise to

A

clone of identical T cells programmed against the same epitope

276
Q

what do the clones of T cells become?

A
  • effector cells
  • cytotoxic cells
  • memory cells
  • helper cells
277
Q

T cell recall response

A

immune memory follows the primary response in cellular immunity

278
Q

why does the T cell recall response occur?

A
  • memory cells are long-lived
  • memory cells are more numerous than naive T cells
  • memory cells have fewer steps to be activated
279
Q

what are the four main steps of T cell activation?

A
  • antigen recognition
  • costimulation
  • clonal selection
  • attack
280
Q

____ play central role in coordinating both cellular and humoral immunity

A

helper T cells

281
Q

what are the three effects that occur when helper T cells secrete interleukins

A
  • attract neutrophils and NK cells
  • attract macrophages, stim their phagocytic activity, and inhibit them from leaving area
  • stim T and B cell nitosis and maturation
282
Q

what happens when T cell recognizes MHC-II

A

secrete interleukins

283
Q

_____ only T cells that directly attack other cells

A

cytotoxic T cells

284
Q

when cytotoxic T cells recognize complex of an antigen and MHC-I what happens

A

it docks on those cells

285
Q

after cytotoxic T cells dicks what happens?

A

cell delivers a lethal hit of chemicals

286
Q

what are the chemicals in a lethal hit?

A
  • perforins and granzymes
  • interferons
  • tumor necrosis factor
287
Q

perforins and granzymes

A

kill cells in the same manner as NK cells

288
Q

interferons

A

inhibit viral replication and recruit and activate macrophages

289
Q

tumor necrosis factor

A

aids in macrophage activation and kills cancer cells

290
Q

what happens after a cytotoxic T cell delivers lethal hit?

A

cell goes off in search of another enemy cell while chemicals do their work

291
Q

B cell activation begins when

A

an antigen binds to B cell receptors

292
Q

___ has thousands of surface receptors for one antigen

A

immunocompetent B cells

293
Q

receptor mediated endocytosis

A

antigen binds to several receptors, links them together, and is taken into the cell

294
Q

What do B cell processes do after the antigen is taken into the cell

A

B cell processes digests the antigen then displays antigen fragments with MHC-II on surface

295
Q

what happens after MHC-II is displayed on surface of B cell

A

secretes interleukins that activate the B cell

296
Q

____ triggers clonal selection

A

B cell activation

297
Q

B cell mitosis gives rise to

A

clones of identical B cells programmed against the same antigen

298
Q

most clonal B cells differentiate into

A

plasma cells

299
Q

what else can B cells become other than plasma cells

A

memory B cells

300
Q

plasma cells secrete

A

antibodies at a rate of 2000 molecules per second

301
Q

what is the lifespan of a plasma cell

A

4-5 days

302
Q

antibodies travel through body in

A

blood and other body fluids

303
Q

first exposure of a plasma cell to antigen triggers

A

production to IgM and a slower production of IgG

304
Q

later exposure of a plasma cell to the same antigen does what?

A

rapid production of IgG

305
Q

antibody assist the immune response in four ways

A
  • neutralization
  • complement fixation
  • agglutination
  • precipitation
306
Q

neutralization as an immune response

A

masking active regions of an antigen

307
Q

complement fixation as immune response

A

activating complement by the classical pathway

308
Q

agglutination as immune response

A

clumping of enemy cells to immobile them

309
Q

agglutination and precipitation cleared by

A

phagocytes

310
Q

precipitation assisting in immune responses

A

antigen molecules are clumped by antibodies

311
Q

primary response

A

immune reaction brought about by the first exposure to an antigen

312
Q

protective antibodies are delayed for ____. Why?

A
  • 3-5 days
  • naive B cells multiply and differentiate into plasma cells
313
Q

as plasma cells produce antibodies what happens?

A

antibody titer rises

314
Q

antibody titer

A

level in the blood plasma

315
Q

what happens to the antibody titer when IgM appears

A

peaks in about 10 days and then soon declines

316
Q

___ levels rise as ___ declines in the primary response

A
  • IgG
  • IgM
317
Q

how long does it take for the IgG level to drop to a low level

A

within a month

318
Q

primary response leaves one with

A

immune memory of the antigen

319
Q

during clonal selection some B cells become

A

memory B cells

320
Q

secondary response

A

immune response when re-exposed to the same antigen

321
Q

memory B cells become plasma cells within hours of

A

reexposure

322
Q

IgG titer does what in secondary response

A

rises sharply an dpeaks in a few days

323
Q

are there symptoms for a secondary response? why?

A

no because response is to rapid that the antigen has little chance to exert noticeable effect on the body

324
Q

IgG remian elevated for how long after secondary response

A

for weeks to years

325
Q

why do IgG remain elevated for so long?

A

long-lasting protection

326
Q

autoimmune diseases

A
  • failure to self tolerance
  • immune system does not correctly distinguish self sntigens from foreign ones and produces auto-antobodies that attack body’s own tissues
327
Q

reasons for failure of self tolerance

A
  • cross-reactivity
  • abnormal exposure of self anitgens to the blood
  • changes in structure of self antigens
328
Q

cross reactivity as a reason for failure to self tolerance

A

some antibodies against foreign antigens react to similar self antigense

329
Q

example of cross reactivity as a reason for failure to self tolerance

A

rheumatic fever where strep antibodies attack the heart valves

330
Q

abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance

A

some of our native antigens are not normally exposed to the blood

331
Q

what is an exmaple of abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance

A

blood testes barrier keep sperm from getting in to the blood

332
Q

changes in structure of self-antigens as reason for failure of self tolerance

A

viruses and drugs may change the structure of self antigens or cause the immune system to perceive them as foreign

333
Q

immunodeficienies are characterized by

A

an immune system that fails to react vigorously enough

334
Q

severe combined immunodificiency disease

A

hereditary lack of T and B cells

335
Q

SCID leaves people vulnerable to

A

oppotunistsic infection

336
Q

aquired immunideficiency syndrome

A

non-hereditary diseases contracted after birth caused by HIV

337
Q

hwo does HIV cause AIDS

A

HIV invades helper T cells, macrophages, and dendritic cells by tricking them to internalize viurses by receptor mediated endocytosis

338
Q

HIV is a

A

retrovius

339
Q

retrovirus

A

uses the viral enzyme reverse transcriptase to convert its viral RNA genome into DNA which can then insert into host cell DNA

340
Q

HIV cripples entire immune system by

A

destorying helper T cellsh

341
Q

host with HIV is most volnerable to

A

opportunistic infections

342
Q

early signs and symptoms of AIDS

A

flu-like symptoms of chills and fever

343
Q

signs and symptoms of AIDS progress into

A
  • night sweats
  • fatigue
  • headache
  • extreme weight loss
  • lymphadenitis
344
Q

what is the normal T helper cell count

A

600-1200 cells/uL

345
Q

what is the T helper cell count in AIDS

A

200 cells/uL

346
Q

what are some opportnistic infections people with AIDS are susceptible to?

A
  • toxoplasma
  • pneumocystis
  • herpes simplex virus
  • cytomegalovirus
  • TB
347
Q

HIV transmitted through

A
  • blood
  • semen
  • veginal secretions
  • breast milk
  • across placenta
348
Q

is there a cure for AIDS

A

no but there is antiretroviral therapy that maintains near normal life expectancy

349
Q

COVID 19

A

global pandemic oc 2020-2021 caused bu SARS-CoV-2

350
Q

viral structure of COVID 19

A

single strand of RNA stabilized by RNA-binding nucleocapsid protein surrounded outer lipid envelope studded with spike proteins

351
Q

how many genes are in the RNA strand of COVID 19

A

14

352
Q

infection cycle of COVID 19

A
  • virus inhaled and invades lung cells
  • virus replicated within host cell
  • new virus released to infect new cells
353
Q

what cells do COVID 19 cells infect and how

A

great (type II) alveolar cells by invading their ACE2 receptors

354
Q

mechanism of COVID 19

A
  • other vody cells with ACE2 receptors also infected
  • cytokines released by immune cells activate inflammation
355
Q

what other body cells have ACE2 receptors

A
  • heart
  • kidneys
  • digestive tract
  • blood vessels
  • brain
356
Q

COVID 19 has the potential to induce a

A

cytokine storm

357
Q

cytokine storm

A

produces excessive hyperinflammatory response

358
Q

common symptoms of COVID 19

A
  • flu-like symptoms
  • loss of smell and taste
  • possible breathing difficulty and low blood oxygen
359
Q

some patients infected by COVID 19 experience

A
  • respiratory failure
  • shock
  • multiorgan dysfunction
360
Q

____ most effective way to prevet critial illness and helt spread fo COVID 19

A

vaccination

361
Q
A

A&P 2 (9 decks)

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