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HLST128: Physiology II > Ch.12 Body Defences > Flashcards

Ch.12 Body Defences Flashcards

1
Q

What are the 5 functions of the immune system

A
  1. eliminate potentially harmful substances
  2. eliminate abnormal and cancerous / mutant cels originally in the body
  3. eliminates foreign / non-self substances
  4. eliminates worn out RBC’s, tissue debris and invading pathogens
  5. allergic responces
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2
Q

what are the malfunction of the immune system

A
  • allergies
  • autoimmune diseases
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3
Q

Example of autoimmune diesease

A
  • Rhematoid arthristis
  • MS
  • Diabetes mellitus
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4
Q

inate defences respond

A

rapidly

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5
Q

Inate defences function

A
  • non specifically defends agains foreign invaders
  • inherited / built in defences
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6
Q

what is used to distiguish invaders as foreign

A

TLR’s

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7
Q

cells of the inate immune system

A
  • neutrophils
  • macrophages
  • basophils
  • natural killers
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8
Q

types of inate defences

A
  • chemical
  • physical
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9
Q

Chemical defences are also called

A

internal defences

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10
Q

types of internal defences

A
  • interferon
  • complement system
  • inflammation
  • natural killer cells
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11
Q

interferon

A
  • non specifically defend against viral infection
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12
Q

complement system

A
  • complements the actions of antibodies to kill foreign cells by forming membrane attack complexes (MAC)
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13
Q

Natural Killer Cells (NK)

A
  • non specifically lyse and destroy virally / cancer infected host cells
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14
Q

purpose of INF

A
  • acts as a wistle blower to warn neighboring cells
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15
Q

Interferon cells process

A
  • virally infected cells relases INF into the ECF which triggers the production of virally blocking enzymes in healthy cells to:
  • breakdown viral mRNA
  • inhibit protein synthesis in host / healthy cells
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16
Q

Function of interferon cells

A
  • breakdown viral mRNA
  • inhibit protein syntheisi in host/ health cells
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17
Q

3 other functions of Interferon

A
  • enhances phagocytic activity and antibody production
  • enhances NK and T lymphocytes, cytotoxic T cells
  • slows cell division and suppress tumor growth
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18
Q

the complement system activiates when

A
  • it is exposed to CHO chains on the surface of a microorganism
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19
Q

the invaders directly _______ the invaders

A

lyse

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20
Q

How is MAC formed? (process)

A
  1. complements (c1 –> plasma protein inactive form)
  2. activates c2, c5, c9
  3. components c5-c9 asseble to form MAC
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21
Q

components _________ assemble to form MAC

A

C5-C9

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22
Q

how do MACS destroy pathogens

A
  • punch holes in the victim surface membrane
  • membrane becomes leaky and causes entry of water through Osmosis
  • causes the cell to burst
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23
Q

what is inflammation
(3points)

A
  • the non specific immune response to foreign material or tissue damage
  • is an essential inate responce to microbial invasion
  • attracts phagocytes and plasma proteins to an invaded or injured area
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24
Q

phagocytes purpose in inflammation (3 points)

A
  • isolate, destroy, or inactivate the invaders
  • remove debris
  • prepare fro sequential sequence and repair
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25
Q

sequence of inflammation

A

defence by resident tissue macrophages –> localized vasodilation –> increased capillary permeability –>localized edema –> walking off inflammed area –>emigiration of leukocytes –> leukocyte proliferation –> markingof destruction of the by Opsin –>leukocyte destruction of cell –>mediation of inflammatory responce by phagocyte secreting chemical –> tissue repair

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26
Q

what is the first step in the inflammation sequence

A

defence by resident tissue macrophages

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27
Q

defence by resident tissue macrophages

A
  • stationary but become mobile units and migrate to invaded tissue –> phagocytose foreign microbes when entering through the skin
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28
Q

what is the second step in the sequence of inflammation

A

localized vasodialtion

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29
Q

localized vasodilation

A

bacterial invasion at the injured site –> attracts most cells –> release histamine –> enhances arteriolar dilation –> attracts more leukocytes and plasma proteins

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30
Q

what is the third step in the inflammation sequence

A

increase capillary permeability

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31
Q

Increased capillary permeability

A
  • mast cells at the injured site relase histamine –> enlarges capillary pores (increases capillaries) –> allows leakage of proteins from the blood to enter the inflamed area
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32
Q

what is the fourth step in the inflammation sequence

A

localized edema

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33
Q

localized edema

A
  • accumulation of plasma proteins in intersticial fluid elevates the local intersticial fluid colloid osmotic pressure —> causes edema —> causes symptoms of inflammation
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34
Q

what does an increased interstical fluid colloid osmotic pressure do

A
  • moves fluid out of the capillay and accumulates at the injured area
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35
Q

edema is

A

swelling

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36
Q

what are the symptoms of inflammation (4)

A
  • redness
  • heat
  • swelling
  • pain
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37
Q

what is the redness caused by

A
  • increased arteriolar vasodilation
  • increased blood delivery
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38
Q

heat is caused by

A
  • increased arteriolar vasodilation
  • increased blood delivery
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39
Q

swelling is casued by

A
  • increase local capillary permuability
  • increased fluid
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40
Q

what is pain caused by

A
  • increased local capillary permeability
    • increased fluids; increased prostaglandin
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41
Q

what do prostaglandin do

A
  • causes attraction of more plasma proteins
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42
Q

what is the fifth step in the inflammation sequence

A

walling off the inflammed area

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43
Q

walling off the inflammed area

A
  • leaked plasma proteins thromboplastin- thrombin and converts fibrogen to fibrin –> this forms a clot around the bacterial invader and damaged tissues
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44
Q

purpose of walling off

A
  • prevents spread
45
Q

what is the sixth step in the inflammation process

A

emigration of leukocytes

46
Q

what are the three step in emigigration of leukocytes

A
  1. margination
  2. dipedsis
  3. chemotaxis
47
Q

margination

A
  • inflammation atraacts neutrophils and monocytes –> attatch to the inner endothelial lining
48
Q

how long does it take for neutrophils to come to the inflmmed area

A

1 hour

49
Q

how long does it take monocytes to come to the inflamed area

A

8 - 12 hrs

50
Q

adhered leukocytes leave capillaries through

A

diapedsis

51
Q

what chemical mediators do inflammed tissues release

A

chemokins

52
Q

how do chemokine attack phagocytic cells

A

chemotaxis

53
Q

chemotaxis

A
  • chemokines bind with receptors on plasma membrane
  • phagocytic cells increases calcium into the cell
54
Q

role of calcium in inflammation

A
  • switches cellular contractile apparatus to lead the crawling of phagocytic cells towards the inflammed tissue
55
Q

what is the 7th step in the sequence of inflammation

A

leukocyte proliferation

56
Q

leukocyte proliferation

A
  • inflammed tissue releases chemical mediators – causes bone marrow to proliferate – large numberof neutrophils, monocytes, and macropages to eliminate invaders and heal tissues
57
Q

what is the 8 step in the sequence of inflammation

A

marking of bacteria for destruction by opsinin

58
Q

marking of bacteria for destruction by opsinin

A

opsin c3-b attatch to TLR’s on phagocytes –> increases phagocytosis by linking foreign cells to a phagoctic cell

59
Q

where is opsin c3-b produced

A

by the liver

60
Q

what is the ninth step in the inflammation sequence

A

leukocyte destruction of the cell

61
Q

leukocyte destruction of the cell

A
  • macrophages and neutrophils release enzymes (lysozomes) to break down and phagocytose the trapped bacteria –> forms pus
62
Q

what is pus

A
  • a collection of dead macrophages, cellular debris, lysozomal phagocytes, and bacteria
63
Q

what is trhe tenth step in the inflammation sequence

A

mediation of the inflammatory responce by phagocyte secreting chemicals

64
Q

mediation of inflammatory responce

A
  • microbe stimulatatinf phagocytes release chemicals / chemokines, which stimulates mediate inflammatory responces
65
Q

mediate inflammatory responces include

A
  • immune activities
  • local responces to systemic manifestation
  • microbal invasion
66
Q

what is the purpose of LEM

A
  • prevent bacterial multiplication
  • stimulates acute phase proteins
67
Q

in which step is LEM secreted

A

10th

68
Q

acute phase proteins include

A
  • interlukin 1 (IL-1)
    – endogenous pyrogens (fever)
69
Q

what is Il-1 secreted by

A

activated macrophages

70
Q

interlukin 1 functions

A
  • proliferation and differentation of the T and B lymphocytes for
  • antibody production
  • cell mediated immunity
71
Q

what is the purpose of an increased temperature in the inflammatory responce

A
  • high temperature interferes with bacterial multiplication
72
Q

when endogenous pyrogens are secreted into the blood it stimulates

A

prostiglandins

73
Q

prostiglandins reach the __________ and stimulate the _______

A
  • hypothalamus
  • thermostat
74
Q

what is the eleventh step in the inflamation sequence

A

tissue repair

75
Q

tissue repair

A
  • fibroblast rapidly divide and secrete large amount of collagen to fill vacated region
76
Q

physical defences are also called

A

external defences

77
Q

what are the two classes of adaptive immunity

A
  • antibody mediated immunity
  • cell mediated immunity
78
Q

antibody mediated immunity is also called

A

humeral immunity

79
Q

antibody mediated immunity involved the productions of _________

A

antibodies

80
Q

humeral immunity involves ____ lymphocytes

A

b

81
Q

B lymphocyte derivatives are known as

A

plasma proteins

82
Q

purpose of B cells

A
  • recognize and respond to bacteria
  • “eye” of the adpative immune system
83
Q

where do B lymphocytes originate

A
  • the red bone marrow
84
Q

plasma cells produce and secrete

A

ImG antibodies

85
Q

when are plamsa cells formed

A

on intitial contact with antigen

86
Q

purpose of plasma cells

A
  • antibody combines with antigen and marks for destruction
87
Q

memory cells can be induced by ________ or ________

A
  • disease
  • vaccination
88
Q

purpose of memeory cells

A
  • provide quicker, more potent, quicker, longer lasting response when faced with the same antigen
89
Q

macrophages are also called

A

antigen presenting cells (APC)

90
Q

what are antigens

A
  • surface protein molecules that marks microbe as a “foreigner”
91
Q

antigens stimulates b cells to

A
  • proliferate and differnetiate into plasma proteins to produce antibodies
92
Q

self antigens cause

A
  • autoimmune diseases
93
Q

what arepurpose of antibodies

A
  • neutralize and aggultinate antigen-antibody complexes and bacterial toxins
94
Q

antibodies are synthesisized by

A
  • plasma proteins in responce to an antigen / foreign material
95
Q

what shape are antibodies

A

y shaped

96
Q

antibodies are coposed of

A
  • four inter-linked polypeptide chains
97
Q

the tails of antibodies are

A
  • fucntional properties
  • the tails are the same in each subclass
98
Q

IgM

A
  • serve as b cell surface recpetor for antigen attatchment
  • secreted in the early stages of plasma celll responce
99
Q

IgG

A
  • most abundant
  • produced when exposed to the same antigen
  • enchances phagocytosis
100
Q

IgE

A
  • protects against parasitic worms
  • immune mediator for common allergic reactions
101
Q

IgA is found in

A
  • found in secretion of digestive, respitory and genitourinary stytem, milk, and tears
102
Q

IgD

A
  • prensent on the surface of many B cells
  • function is uncertain
103
Q

what antibodies are responsible for most specific immune responses

A
  • IgM
  • IgG
104
Q

what are the tree steps in antibody neutralization / aggulation

A
  • aggualtion
  • precipitation
  • neutralization
105
Q

agglutination

A
  • foreign cells or mismatched tranfused RBC’s bind together as a clump
106
Q

precipitation

A
  • antigen-antibody complexes invlove soluable antigens (tenus toxins), lattices / chains become large and precipitate out of the solution
107
Q

what is an example of a soluable antigen

A

tetnus toxins

108
Q

neutralization

A
  • prevent toxins from entering neighboring cells
  • prevent some antigens from excreting their dentrmental effects
109
Q

antigen - antibody complexes

A
  • binding cross links numerous antigens into chains / lattices

HLST128: Physiology II (14 decks)

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