Powerpoint-Chap2 Flashcards
1
Q
What are the acute inflammatory cell
A
granulocytes
2
Q
What are the 3 main involvements of acute inflammation
A
vascular dilation and increased flow
microvasculature alterations to allow egress of cells and proteins
emigration, accumulation and activation of leukocytes
3
Q
What are the 4 cardinal signs of inflammation
A
dolor-pain
calor-heat
rubor-redness
tumor-swelling
4
Q
What is the 5th cardinal sign of acute inflammation
A
functio laesa-loss of function
5
Q
What is the Lewis Triple response
A
red line(vasodilation)
red flare- after 15-30 seconds (vasodilation)
wheal in 1-3 minutes (vascular leakage)
6
Q
what cells release histamine
A
mast cells
7
Q
how can we completely stop inflammation
A
cutting the nerves involved
8
Q
What can cause acute inflammation
A
infections, necrotic tissues, hypoxia, foreign bodies, immune reactions
9
Q
what factor during hypoxia causes inflammation
A
hypoxic induced factor 1 alpha
10
Q
what is released in necrotic tissue to cause inflammation
A
uric acid, ATP, HMGB-1 DNA
11
Q
what are the main triggers of inflammation in an infection(foreign)
A
toll like R and cytoplasmic R
12
Q
In a blood smear describe what neutrophils look like
A
have 3+ nuclei usually. young neutrophils have the banded nucleus
13
Q
In a blood smear what do the eosinophils look like
A
hace 2 nuclei usually
14
Q
In a blood smear what do the basophils look like
A
stain darker and very punctuated
15
Q
What do the lymphocytes look like in blood smear? how do you tell them from monocytes
A
have oval purple nucleus
monocytes stain lighter, and have more cytoplasm(nucleus usually kidney shaped
16
Q
What are majority of cells in a virus caused inflammation
A
lymphocytes
17
Q
what are majority of cells in a pseudomonas caused reaction
A
neutrophil dominance
18
Q
what is the normal pattern of cell population in acute inflammation
A
granulocytes early followed by monocytes
neutrophils followed by macrophages
19
Q
What chemical mediators cause vascular permeability
A
histamine, bradykinin and leukotrienes
20
Q
what is exudation and what causes it
A
fluid, proteins, RBC and WBC in intravascular space as a resuls of increased osmotic pressure extravascular, and increased hydrostatic pressure intravascular
21
Q
What is vascular stasis
A
slowing of blood with vasodilation and fluid exudation to allow chemical mediators and inflammatory cells to collect and respond to stimulus
22
Q
what 2 componenets contribute to vascular stasis
A
less blood (fluid loss) and vasodilation
23
Q
what is the term margination
A
leukocytes accumulating on vascular endothelium
24
Q
What are the two manifestations from vasodilation
A
erythema and warmth
25
what is histamines mechanism that leads to vascular permeability
causes endothelial cells to contract and so then there are gaps between cells
26
What are the other chemicals that increase vascular permeability
NO and VEGF
27
WBC have what barrier to escape through when endothelial cells contract and make pathways
basement membrane
| have collagenase to chew through
28
what is transudate
ultrafiltrate of plasma leaking from vessls due to increase hydrostatic P or decrease P
29
what is exudate
mixture of cells and plasma leaking out of vessels in response to chemical mediators
30
What is purulent exudate
granulocyte rich, cellular debris, +/- microbes (pus)
31
Why is the nucleus on one side of the cell in a plasma cell
because rER is so large, squishes nucleus over to one side
32
what causes fibrinous pericarditis
exudate
33
What are the types of body cavity effusion
```
serous- yellow/clear
serosanguinous- mixed
sanguinous- blood
purulent
chylous
```
34
white and milky effusion is called what
chylous
35
which is more alkaline, transudate or exudate
transudate
36
if pressure increases in body, like increased Cardiac output, what leaks out
fluid- transudate
37
inflammation and increased P, what will leak out of cells
exudate- proteins, enzymes, maybe bacteria. Acidic. maybe odorous
38
what is dermatographism a reaction to
histamine. when we scratch ourselves and redness and wheal forms. this is when it lasts for more than 30 minutes
39
what is the immediate transient response
the leakage of histamines because vasodilation and endothelial cells contract. 15-30 minutes
No neutrophils!
40
What is the immediate sustained response
thermal chemical burns or lytic bacterial infection
leakage starts and lasts several hours to days
endothelial cell necrosis occurs
venules, capillaries and arterioles may be affected
41
What is delayed prolonged leakage
leakage 2-12 hours after injury
inflammation lasts hours to days
bacterial toxins, mild to moderate thermal burns
capillaries and venules affected- mechanism unclear
42
How does leakage drain
lymphatics
43
what is lymphangitis
inflammation of lymph vessels
44
what is lymphadenitis
inflammation of vessels and lymph nodes
45
what is adenitis
inflammation of lymph node
46
what are the steps in leukocyte emigration
stasis- margination- rolling- adhesion- migration
47
how do leukocytes migrate across the endothelium
chemotaxis towards concentration gradient
48
how do leukocytes migrate across basement membrane
chemotaxis, cytoskeleton, collagenases
49
how do leukocytes migrate into tissues
chemotaxis, integrins and CD44
50
what occurs first in leukocyte migration, crossing endothelium or basement membrane
crossing endothelium
51
TNF and IL1 increase expression of what on endothelium
P selectin, E selectin and integrin ligand (CAM1)
52
what cell has a weibel palade bodies
endothelial cells
53
Where is L selectin located
on the leukocyte
54
recurrent bacterial infections(not pustular), periodontitis and impaired wound healing are key to what pathology
rare, deficiencies in leukocyte adhesion molecules
55
What is CD99
normally repulses cells but changes to homophillic state and allows leukocytes to migrate through endothelial cells
56
When neutrophils bind and the GPCR is activated what occurs
increase Ca, kinases causing polymerization of actin (filopodia) can move towards signals
57
what are chemoattractants
cytokines, complement C5a, leukotriene B4
| bacterial products
58
which complement component is chemotactic
C5a
59
what are the humoral endogenous chemotactic factors
fibrin split products (PMNs)
| complement C5a and C567
60
What cells can be phagocytes
macrophages
| neutrophils
61
what do phagocyte WBC recognize on targets
mannose R
scavenger R- LDL
opsonins
62
what does a classically activate macrophage do
kill bacteria
63
what do alternatively activated macrophages do
wound repair and anti-inflammatory
64
What are the antiinflammatory substances secreted from macrophages
IL10 and TGF beta
65
Chronic arthritis is due to what cells and molecules
lymphocytes macrophages and antibodies
66
chronic atherosclerosis is from what cells
macrophages and lymphocytes
67
what cells are responsible for chronic transplant rejection
lymphocytes and cytokines
68
what cells are responsible for pulmonary fibrosis
macrophages and fibroblasts
69
what cell is responsible for lug abscess
neutrophils
70
what chemicals are responsible for septic shock
cytokines
71
what cells and molecules are responsible for acute transplant rejection
lymphocytes, Ab and complement
72
what cells are responsible for acute respiratory distress sydnrome
neutrophils
73
What is chediak higashi syndrome
lysosome fusion disorder. phagolysosomes
74
what are problems with leukocytes with microbial activities. (deficiency)
decreased phagocyte oxidase leading to dec in ROS and results in chronic granulomatous disease and decreased MPO leading to recurrent candida infections
75
What type of diseases have impaired WBC production
bone marrow suppression, tumors, radiation and chemotherapy
76
what are our innate mechanisms to end acute response
mediators and neutrophils have short half lives
77
what are the active mechanisms in our bodies to end acute response
switch AA products
liberation of anti-inflammatory cytokines TGFb
prduction of anti-inflammatory lipid mediators (resolvins and protections)
neural changes (dec TNF by macrophages)
78
Describe how cell derived chemical mediators of inflammation are made
preformed or newly synthesized by simple splice to activate
79
what are the plasma derived mediators of inflammation
coagulation
complement and kinin
activation of normally present proteins by cascades
80
what cells make histamine
mast cells, basophils and platelets
81
what cell release serotonin
platelets and neuroendocrine cells
82
What cell releases NO
macrophages and the endothelium
83
What factor in coagulation cascade is key to set everything off
factor XII
84
what does serotonin do for inflammation
vasodilation, increased vascular permeability
85
What cells release TNF and IL 1
macrophages, endothelial cells and mast cells
86
where are complement and kinins produced
in the liver
87
what causes release of histamine
```
physical injury (triple response)
neuropeptides (subP)
Ab binding
anaphylatoxins (C3a and C5a)
leukocyte histamine releasing proteins
cytokines (IL1 and IL8)
```
88
serotonin has similar activity to what other mediator
histamine
89
What R does histamine worked through
H1 R on endothelial cells
90
what are the primary roles of histamine
constrict large arteries
vasodilation
increase venular permeability via endothelial contraction
91
What inactivates histamine
histaminase
92
What sets off serotonin release
collagen, thrombin, ADP and Antigen Ab complexes
93
What are eicasanoids
AA metabolites
94
steroids inhibit what
phospholipases which make AA
95
Cox1 and 2 inhibitors block what
cyclooxygenase
96
Prostaglandin is converted into what
prostacyclin and thromboxane A2
97
what is the role of prostacyclin
vasodilation, inhibits platelet aggregation
98
what is the role of thromboxane A2
vasoconstriction, promotes platelet aggregation
99
What are derivatives produced via cycloocygenases
thromboxane A2
prostacycline
PGD2
PGE2 and PGF2
100
what is the effect of PGE2
pain and vasodilates
101
What does PGD2 cause
attracts neutrophils, vasodilates
| pain and fever via cAMP action on temp set point
102
What do leukotrienes cause
bronchoconstriction, increase vascular permeability
cause vasoconstriction
attract leukocytes
103
what do lipoxins do
inhibit leukocyte recruitment and inflammation
104
Which leukotriene is responsible to attract leukocytes
B4
105
What do aspiring and other NSAIDs inhibit
Cox1 and 2
106
cox 1 makes what
thromboxane
107
cox 2 makes what
prostacyclines
108
cox 2 inhibitors impair what
endothelial cell production or prostacyclin (which is a vasodilator and inhibitor of platelet aggregation)
109
what is the problem with cox 2 inhibitors
increase risk of clot because cox1 unnopposed
110
lipoxogenase inhibitors are used for what
asthma
111
What cells make platelet activating factor
platelet, endothelial cells and leukocytes
112
what activates release of platelet activating factor
platelet aggregation, vasoconstriction, bronchoconstriction
enhanced leukocyte adhesion
at low concentrations causes vasodilation
113
What are the primary reactive species
O2-, H2O2, and OHelctron
114
when reactive species combine with NO what is product
ONOO electron
115
what causes ROS
endothelial cell damage
damage to parenchymal cells and erythrocytes
inactivate proteases
116
smoking kills what protein
alpha1 antitrypsin
117
What is the role of NO
relaxes smooth m
inhibits leukocyte rolling, adhesion and degranulation
inhibits platelet aggregation and adhesion
inhibits mast cell activated inflammation
118
What are the 3 types of nitrous oxide synthetase
constituitive: endothelial eNOS and Neuronal nNOS
| inducible (iNOS) from monocytes and macrophages activated by TNF and INF gamma
119
what are cytokines
general category of messenger molecules
120
what are chemokines
special cytokines that direct leukocyte migration
121
How do chemokines work
bind to GPCRs
122
What activates TNF and IL 1
macrophages
123
What controls IL 1 production
inflammasome
124
what is the action of TNF and IL 1 generally
endothelial activation to activate adhesion molecules in the acute phase, fever and also activates fibroblasts and nuetrophils
125
Increased active IL 1 with mutation result in what
inherited autoinflammatory syndromes
126
Which cytokine is responsible for cachexia when sick( don't want to eat)
TNF
127
what is happens to iron when we are sick
more hepcidin available which binds up all the iron. so looks like iron deficient(anemia) but not really
128
What are the azurophil granules
primary neutrophils that show up first
129
what are the specific granules(neutrophil)
secondary, show up second
130
What type of enzymes are in specific granules
more enzymes for digestion, like collagenase, lysozyme
131
What reaction is substance P known for
wheal formation
132
where are majority of neurons with substance P located
GI tract and lungs
133
what does sub P cause
pain, endocrine cells secretion, mast cell activation, vascular permeability
134
What is hageman factor XII involved in
activates clotting cascade, kinin cascade, fibrinolytic cascade, complement cascade
135
What do fibrin split products produce
chemostasis, inflammation
136
Which cascade results in production of bradykinin? what is bradykinins role
the kinin cascade from kallikrein make bradykinin
| bradykinin activates C5 to C5a which causes more inflammation
137
plasmin has what affect on complement
splits C3 into C3a and b
138
Which Complement parts make MAC
C5b-Cp
139
What are the anaphylatoxins of complement cascade
C3a, C4a and C5a
140
what else does C5a do
leukocyte activation
chemotaxis
lipoxygenase increased activity
141
which complement parts are opsonins
C3b and iC3b
142
What do protease activated receptors cause
```
mobilization P selectin
chemokine production
Cox2 induction
increased PGs PAF and NO
endothelial adhesion
endothelial conformation change
```
143
what are the actions of bradykinin
increased vascular permeability
smooth m contraction
pain
144
what is the role of kallikrein
positive feedback to XII, creates bradykinin
145
What is the role of plasmin in the fibrinolytic system of inflmmation
breaks down fibrin into split products
increase vasc permeability
chemotactic for leukocytes
146
what is the role of an anaphylatoxin
release histamine
147
What mediators play a role in vasodilation
PGs NO and histamine
148
what mediators increase vasc permeability
histamine, serotonin, C3a C5a bradykinin Leukotrienes
| PAG and sub P
149
what mediators are included in chemotaxis
TNF IL 1 chemokines, C3a C5a leukotriene B4
150
What mediators induce fever
IL 1 TNF and PGs, PGE2!
151
what mediators induce pain
PGs and bradykinin!!!
152
what mediators induce tissue damage
lysosomal enzymes of leukocytes
ROS
NO
153
what is resolution
complete repair after inflammation
154
What is fibrosis from inflammation
collagen deposition and loss of function
155
if inflammation never goes away what is the problem
chronic inflammation
156
What is exudative acute inflammation
stuff coming out
157
what is serous inflammation
serous fluid coming out
158
what is fibrinoid vs fibrinous
fibrinous we can see it
| fibrinoid is under microscope
159
urticarial inflammation means what
itchy
160
what is catarrhal inflammation
runny nose
161
What is cellulitis
inflammation of skin
162
what is necrotizing inflammation
necrotic inflammatory process
163
what type of inflammation is granulomatous
chronic
164
what is interstitial inflammation
in between layers
| acute or chronic
165
what is cytopathic inflammation
cell has been modified- like in viruses
166
what is purulent vs serous
serous clear yellow
| purulent- pus
167
pericarditis and endocarditis are examples of what inflammation
fibrinous
168
what does fibrinous inflammation look like under scope
very pink- lots of protein, lots of fibrin
169
what is pseudomembranous inflammation
form of exudative inflammation involving mucous and serous membranes
fibrin in exudate causes membrane like covering that is adherent to inflamed tissue
170
what types of infections cause pseudomembranous inflammation
c difficile colitis
| corynebacterium diptheriae pharyngitis
171
what are mononuclear cell infiltrates in chronic inflammation
macrophages, lymphocytes, plasma cells, other cells
172
what does chronic inflammation arise from
continued infections
prolonged exposure to toxic/foreign agents
autoimmune diseases
malignancies
173
In acute viral infections what happens to neutrophil count
neutrophils go down. lymphocytes up
174
what are the characteristics of chronic inflammation
chronic inflammatory cells
| destruction of parenchyma and replacement by CT
175
Describe life of monocytes
live in blood 1 day unless activated into macrophages which can live longer
176
What is the hallmark of chronic inflammation
tissue damage
177
What are the macrophages of body
```
alveolar macrophages in lungs
microglia in CNS
kupffer in liver
osteoclasts in bone
dendritic cells of many tissues
langerhans are the dendritic cells of the skin
```
178
what are the 2 roles of macrophages
increase inflammation or begin repair
179
Why are benign cells found surrounding malignant cell
all the cehmoattractancts that the malignant cell is releasing
180
what is the perinuclear huff
the edge of the plasma cell that is dark around cytoplasm
181
what are produced in eosinophils
IL 3, IL 5
| granulocyte/monocyte colony stim factor GM-CSF
182
what are the chemoattractans for eosinphils
LTB4, CCL5(RANTES) and eotaxin 1 and 2
183
what are in the granules in eosinophils
```
basic protein(toxic to parasites)
cytotoxic agents like cationic proteins, neurotoxin and peroxidase
```
184
Which parasites that get attacked by eosinophils
helminths
185
what is the most common cause eosinophilia
allergies
186
How do you know if a cell is a basophil
cannot see the nucleus because it is so dark
187
what are the main components that are staining dark in basophils
histamine and heparin
188
big cell lots of cytoplasm
macrophages
189
what is the most common granulomatous disease
TB
190
If the nuclei of a giant cell are around the edge what are they called
langhans type giant cell
191
Describe histo sarcoidosis
granulomas
no central necrosis like we see in TB
mainly macrophages
192
describe difference of cat scratch fever compared to other granulomas
has neutrophils in the areas as well
193
What cytokines are responsible for fever in inflammation
IL1 IL 6 TNF and IFN gamma
194
What cytokines are generated in large amounts that causes sepsis
TNF IL1
195
what is neutropneia or agranulocytosis
too few circulating neutrophils
196
What can cause neutrophil adherence molecule problems
hereditary, DM, glucocorticoid admin, ehtanol
197
what chronic disease can cause failure of neutrophils to move properly
DM
198
what can cause failure of neutrophils to phagocytose
DM, complement of Ig deficiencies
199
Insufficient Oxygen radicals can lead to what type diseases
chronic granulomatous diseases
200
Major burns can cause what deficiency
chemotaxis
201
what can lead to deficiencies in phagocytosis and microbial activity
leukemia, anemia, sepsis, DM, neonates and malnutrition
