Chapter 2 Flashcards
(144 cards)
1
Q
what are the three functions of inflammation?
A
- killing of microbes 2. removal of cellular debris 3. initiates repair
2
Q
true or false. our bodies can heal without inflammation.
A
false
3
Q
what drug will prevent inflammation and sensing pain?
A
corticosteroids
4
Q
how long do lymphocytes last in blood and lymph?
A
about 4 days (short time)
5
Q
where are leukocytes made?
A
bone marroe
6
Q
what are the 5 types of WBCs?
A
- lymphocytes 2. monocytes 3. neutrophils 4. eosinophils 5. basophils
7
Q
what are the 3 types of lymphocytes?
A
B cells, T cells, Natural Killer (NK) cells
8
Q
what type of lymphocyte make plasma cells and which make antibodies?
A
B cells
9
Q
what leukocyte will eventually become a macrophage?
A
monocyte
10
Q
what type of WBC contains histamine?
A
neutrophil
11
Q
what are the three types of granulocytes?
A
- neutrophils 2. eosinophils 3. basophils
12
Q
what are the two types of agranulocytes?
A
- lymphocytes 2. monocytes
13
Q
where are plasma proteins made?
A
liver
14
Q
how does inflammation eliminate infection and damaged tissue?
A
it attracts WBCs and circulates them to the target tissue
15
Q
what are the 3 types of secondary tissue damage?
A
- violent microbes (tuberculosis, HIV) 2. chronic inflammation 3. hypersensitivity rxn (anaphylactic shock, autoimmune rxns)
16
Q
injury or infection is detected via what three cells?
A
macrophages, dendritic cells, mast cells
17
Q
how do macrophages, dendritic cells, and mast cells induce inflammation?
A
secretes cytokines
18
Q
what are the 5 cardinal signs of acute inflammation?
A
redness, heat, swelling, pain, loss of function
19
Q
what are the 5 R’s of inflammation?
A
- recognize 2. recruit 3. remove 4. regulate 5. resolution
20
Q
true or false. inflammation is typically long and self-limited.
A
false. short-lived and self limited
21
Q
during inflammation, are pro-inflammatory mediators inactivated or activated?
A
inactivated
22
Q
during inflammation, are anti-inflammatory mediators inactivated or activated?
A
activated
23
Q
what are two types of inflammation?
A
acute and chronic
24
Q
describe acute inflammation.
A
sudden onset, obvi local signs, neutrophils, no time for scar tissue
25
describe chronic inflammation.
gradual onset, few local signs, macrophages and lymphocytes
26
what are the 2 major components of acute inflammation?
1. vascular changes 2. WBC recruitment
27
what are some examples of acute inflammation stimuli?
infection, trauma, ischemia, necrosis, foreign bodies, hypersensitivity reactions
28
what two cells are associated with acute inflammation and what is their function?
neutrophils and plasma proteins destroy microbes and cellular debris
29
what are the two pattern recognition receptors in acute inflammation?
1. toll-like receptors 2. inflammasome
30
true or false. toll-like receptors are found on the inside on the lipid bilayer (plasma membrane).
false. outside
31
what is the location of inflammasome?
cytosol
32
what is the function of toll-like receptors? inflammasome?
recognize all types of infectious pathogens; recognize dead cell products (crystals ATP)
33
what are two functions of pattern recognition receptors?
1. recognize harmful agents 2. identify molecular patters as "non-self"
34
what are the three types of vascular changes that alter caliber and permeability?
1. vasoconstriction 2. vasodilation 3. increased vessel permeability
35
true or false. vasoconstriction last at least a minute during vascular changes.
false. a few seconds
36
what does vasodilation do during vascular changes?
increase blood flow (prolonged) = redness and warmth
37
what is the purpose of increasing vessel permeability during vascular changes?
fluid to target tissues; increase viscosity -->stasis-->WBCs collect along vascular wall--> diapedesis
38
what is the term associated with WBCs collecting along the vascular wall?
margination
39
what is another term for migration/WBC squeezing through wall?
diapedesis
40
what are the 3 mechanisms of vascular changes that increase the permeability and reverses osmotic gradients?
1. endothelial contraction 2. endothelial necrosis 3. angiogenesis
41
what is the most common vascular change that increases permeability and reverses osmotic gradients?
endothelial contraction
42
what happens during endothelial contraction?
histamine binds which leads to gaps in postcapillary venules (short lived)
43
true or false. endothelial necrosis is not leaky.
false. leaky until repaired
44
what are some types of endothelial necrosis?
burns, severe infections, irradiation
45
true or false. angiogenesis is the formation of new vessels with leaky endothelial cells.
true
46
true or false. WBC leave circulation through arteriole side and fluid leaves through venous side.
true
47
what are the two types of edema in acute inflammation?
exudate and transudate
48
when does edema develop?
when lymphatic drainage cannot keep up
49
what are the 3 types of lymphatic responses?
1. lymphadenopathy 2. lymphadenitis 3. lymphangitis
50
define lymphadenopathy.
general disorder of lymph nodes
51
define lymphadenitis.
inflamed notes, increased size and pain, can lead to shock
52
define lymphangitis.
inflamed lymphatic channel
53
what are the 4 steps in leukocyte recruitment?
1. margination 2. firm adhesion 3. diapedesis 4. chemotaxis
54
margination is mediation by _______.
selectins
55
firm adhesion is mediated by ______.
integrins
56
migration via pseudopodia during leukocyte activation is stimulated by what?
bacterial, cytokines, complement
57
what leukocyte predominates acute inflammation?
neutrophils
58
neutrophils are killed within 48 hours via apoptosis and are replaced by what two cells?
macrophages and lymphocytes
59
what are the stimuli for leukocyte activation?
microbes, necrotic tissue, foreign bodies
60
define opsonization.
sticking an antibody on surface in order to hunt down and destroy
61
what are the two mechanisms for phagocytosis?
1. opsonization 2. engulfment and degradation
62
what are the two opsonins for opsonization?
antibodies (IgG) and complement proteins
63
what is the function of opsonins?
enhance macrophage binding and breakdown
64
what are the 3 inadvertent damages to normal cells (secondary tissue injury)?
1. persistent infections 2. ischemia reperfusion injuries 3. hypersensitivity reactions
65
what are examples of persistent infections during leukocyte-induced tissue injury?
tuberculosis and viral infections (HIV)
66
what are the three outcomes of acute inflammation?
1. resolution 2. chronic inflammation 3. scarring
67
true or false. chronic inflammation does not lead to scarring.
false
68
of the three outcomes of acute inflammation, which one is a minimal injury and which one is a severe injury?
minimal- resolution; severe-scarring
69
what are the 6 types of patterns of inflammation?
1. serous 2. fibrinous 3. suppurative 4. ulcerative 5. pseudomembranous 6. granulomatous
70
what type of inflammation pattern accumulates serum within or below the epidermis and has a watery effusion?
serous
71
what are 3 causes of serous inflammation?
autoimmune, chemical exposure, poison ivy
72
what inflammation pattern is due to severe injury and will increase vessel permeability?
fibrinous
73
what will fibrinous inflammation produce?
fibrin rich exudate
74
where will fibrinous inflammation occur?
pericarditis and pleuritis
75
what type of inflammation patter is a local infection with pus forming organism?
suppurative
76
what constitutes pus?
neutrophils, dead/injured tissues, edema
77
what is an abscess?
localized pus
78
define ulcerative inflammation.
superficial area of necrotic tissue
79
what are some types of ulcerative inflammation?
peptic and aphthous ulcers
80
what are 2 types of pseudomembranous inflammation?
dipthriae and C-Diff
81
what is another name for suppurative inflammation?
purulent
82
where will you find fibrinous inflammation?
heart and lungs
83
where will you find purulent/suppurative inflammation?
skin/acne
84
what inflammation pattern is a pattern of chronic inflammation?
granuloma
85
true or false. there are few scattered lymphocytes among the macrophages in granulomas.
true
86
what is the main condition that produces granulomas?
tuberculosis
87
what type of granuloma does tuberculosis create?
caseating granuloma
88
true or false. fungal infection in the lungs are common and symptomatic.
false. a-symptomatic
89
what are the 6 cell derived mediators of inflammation?
1. vasoactive amines 2. arachidonic acid metabolites 3. cytokines 4. reactive oxygen species 5. lysosomal enzymes 6. neuropeptides
90
what is released from vasoactive amines and what are their functions?
histamine- vasodilation and serotonin-vasoconstriction during clotting
91
where do vasoactive amines come from?
mast cells and platelets
92
what type of inflammation do vasoactive amines function in?
acute
93
where do arachidonic acid metabolites come from?
WBCs, mast cells, endothelia, platelets
94
what three things are secreted from arachidonic acid metabolites?
prostaglandins, leukotrienes, lipoxins
95
what is the function on prostaglandins?
vasodilation, pain, and fever
96
what will block prostaglandin synthesis?
NSAIDs= reduced pain and fever
97
what is the function of leukotrienes?
bronchospasm and increase permeability
98
what is the function of lipoxins?
inhibit chemotaxis (anti-inflammatory)
99
where do cytokines come from?
mast and endothelial cells, macrophages
100
what is the function of cytokines?
increase WBC production, adhesion, and migration
101
true or false. cytokines are anti inflammatory.
false. pro inflammatory
102
where do reactive oxygen species comes from?
neutrophils and macrophages
103
what is secreted from ROS? what is the function?
Nitric Oxide; vasodilation and microbial killing
104
where will you find lysosomal enzymes?
within neutrophils and monocytes
105
what is the function of lysosomal enzymes?
microbial killing and tissue degradation
106
what is the function of neuropeptides?
initiate inflammation, transmit pain, and regulates vascular tone and permeability
107
substance p is released from which inflammation mediator?
neuropeptides
108
what are the three plasma protein derived inflammation mediators?
1. complement proteins 2. coagulation proteins 3. kinin system
109
what plasma protein derivative deals with opsonization, increase permeability, WBC adhesion, and chemotaxis?
complement proteins
110
membrane attack complex deals with bacteria under what inflammatory mediator?
complement proteins
111
Hageman factor from the liver deals with what plasma protein derivative?
coagulative proteins
112
coagulative proteins activate _____ which leads to clotting.
thrombin
113
true or false. coagulative proteins will only stimulate kinin systems.
false. it will stimulate complement and kinin systems
114
kinin system is a plasma protein derivative that will lead to the production of ______?
bradykinin
115
what is the function of bradykinin?
vasodilation, pain, and coagulation
116
what is chronic inflammation due to?
unresolved acute inflammation
117
what are the 3 causes of unresolved acute inflammation?
1. prolonged inflammation 2. immunosuppression 3. hypersensitivity
118
what are the 3 features of chronic inflammation?
1. mononuclear leukocytes (macrophages, lymphocytes, plasma cells) 2. tissue destruction 3. vessel production and fibrosis
119
what cell is the dominant cell at the site of chronic inflammation?
macrophages
120
what are the 2 functions of macrophages?
1. eliminate microbes and dead cells 2. initiate angiogenesis and fibrosis
121
what are macrophages activated by?
edotoxin, cytokines, foreign bodies
122
what cell of chronic inflammation deal with innate and adaptive immunity?
lymphocytes
123
why do b cells produce plasma cells to produce antibodies?
so we an have a faster reaction next time
124
what cells are associated with alternatively activated macrophages?
mast cell and eosinophils
125
what do leukocytes produce?
cytokines
126
what are the two systemic effects of inflammation?
fever and elevated plasma proteins
127
fever and elevated plasma proteins are associated with what type of reaction?
acute phase reaction
128
what are some symptoms of acute phase rxn?
lethargy, somnolence, malaise, increase HR and BP, anorexia, anhidrosis (lack of sweating)
129
fever is associated with what part of the brain?
hypothalamus- increase temp set point (feel cold)
130
what will lead to prostaglandin synthesis during fever?
pyrogens
131
what will lead to inflammation during elevated plasma proteins?
increased CRP and fibrinogen and increased ESR of Sed Rate
132
define leukocytosis.
elevated leukocytes in blood
133
leukocytosis commonly follows infections. bacterial will increase ______ and viral will increase _______.
neutrophils; lymphocytes
134
leukemoid rxns mimic _______.
leukemia
135
what is the term associated with a decrease in blood leukocyte count?
leukopenia
136
what are some causes of leukopenia?
AIDS, chemotherapy, radiation
137
what are some various sources of cell injury?
trauma, microbial infections, foreign bodies, toxins, chronic inflammation
138
true or false. tissue repair begins after inflammation is eliminated.
false. before
139
what is the difference between regeneration and scarring?
regeneration- stem cells proiferate; scarring- cells are unable to proliferate
140
where can you find fibrosis?
lungs, liver, kidney, myocardium
141
fibrosis occurs in tissues with what two features?
1. chronic inflammation 2. damage to terminally differentiated cells (mature)
142
what are examples of terminally differentiated cells?
CNS neurons and cardiac myocytes
143
how are cell and tissue regeneration stimulated by growth factors?
production of GFs and cellular response to GF (entry into cell)
144
what three factors are needed for tissue homeostasis?
1. cellular proliferation 2. apoptosis 2. stem cell differentiation
