Imflammation I Flashcards
(87 cards)
1
Q
Components of innate immunity (school)
A
Natural Killer cells
Dendritic cells
Epithelial cells
Proteins of the complement system
2
Q
What cells provide first response to infection (apart from leukocytes)
A
Components of innate immunity
3
Q
Sequence of events in inflammatory reaction
A
- Macrophage recognition
- Clotting begins
- Chemokines attract phagocytic cells to injury site
- Neutrophils and macrophages phagocytose pathogens
- Tissue heals
4
Q
Acute disorders caused by inflammatory reactions
A
- Acute respiratory distress syndrome
- Asthma
- Glomerulonephritis
- Septic shock
5
Q
Cells involved in acute respiratory distress syndrome
A
Neutrophils
6
Q
Cells involved in asthma
A
Eosinophils; IgE antibodies
7
Q
Cells involved in glomerulonephritis
A
Antibodies and complement; neutrophils and monocytes
8
Q
Cells involved in septic shock
A
Cytokines
9
Q
Chronic diseases caused by inflammatory reactions
A
Arthritis
Asthma
Atherosclerosis
Pulmonary fibrosis
10
Q
Cells involved in arthritis
A
Lymphocytes, macrophages; antibodies
11
Q
Cells involved in atherosclerosis
A
Macrophages; Lymphocytes
12
Q
Cells involved in Pulmonary fibrosis
A
Macrophages; fibroblasts
13
Q
What are the main characteristics of acute inflammation
A
- Exudation of fluid and plasma proteins (edema)
- Emigration of leukocytes, predominantly neutrophils
14
Q
Which phase of inflammation is associated with ‘more tissue destruction’
A
Chronic
15
Q
Cardinal signs of inflammation
A
Rubor
Tumor
Calor
Dolor
Functio laesa
16
Q
Causes of inflammation
A
- Infections
- Tissue Necrosis
- Foreign bodies
- Deposition of endogenous substances
- Immune reactions
17
Q
Three major components of AI
A
- Dilation of small vessels
- Increased permeability of the microvasculature
- Emigration of the leukocytes from microcirculation, accumulation at site and activation.
18
Q
What is an exudate
A
An extra vascular fluid that has a high protein concentration and contains cellular debris
19
Q
What is a transudate
A
A fluid with low protein content(most of which is albumin), low or no cellular debris and low specific gravity
20
Q
An ultra filtrate of blood plasma that is as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability
A
Transudate
21
Q
Edema can be either an exudate or a transudate T/F
A
T
22
Q
Pus is rich in
A
Leukocytes (neutrophils)
Debris of dead cells
Microbes
23
Q
What are the states of the pressures involved in transudate production
A
- Increased hydrostatic pressure (venous outflow obstruction eg congestive heart failure)
- Decreased colloid osmotic pressure (decreased protein synthesis eg liver disease); (increased protein loss eg kidney disease)
24
Q
There’s vasodilation and stasis in exudate production T/F
A
T
25
There’s increased interendothelial spaces in transudate formation T/F
F. Increased interendothelial spaces in exudate formation
26
Vasodilation is mediated by
Histamine
27
What vessels are affected in AI vasodilation
Arterioles
Capillaries
28
In acute inflammation, blood flow is *increased/decreased/normal*
Increased
29
Following vasodilation in acute inflammation, there’s outpouring of fluid into the extra vascular tissues. This fluid is called
Exudate. Protein rich fluid
30
Loss of fluid and increased vessel diameter lead to (3)
Slower blood flow
Concentration of red cells in small vessels
Increased viscosity of blood
31
As stasis develops, what occurs with neutrophils
They accumulate along the vascular endothelium
32
Mechanisms responsible for increased permeability of post capillary venules
1. Contraction of endothelial cells (leakage)
2. Endothelial injury
3. Transcytosis
33
Contraction of endothelial cells is elicited by
Histamine
Bradykinin
Leukotrienes
Other mediators
34
What is called the immediate transient response
Contraction of endothelial cells (vascular leakage)
35
Contraction of endothelial cells (vascular leakage) usually lasts for how long
15-30 minutes
36
In some forms of mild injury, vascular leakage begins after a delay of 2-12hrs and lasts hours or days T/F
T
37
Late appearing sunburn is a good example of what type of leakage
Delayed prolonged leakage
38
Endothelial injury can lead to
Endothelial cell necrosis and detachment
39
Direct damage to the endothelium can be caused by
1. Sever injury e.g burns
2. Induced by the actions of microbes and microbial toxins that target endothelial cells
40
Transcytosis (increased transport of fluids and proteins through the endothelial cell) may involve
Intracellular channels stimulated by VGEF(vascular endothelial growth factor)
41
In late stages of inflammation, neutrophils that adhere to the endothelium may also injure the endothelial cells T/F
T
42
The constellation of pathologic changes that occur in lymphatic vessels and nodes is termed
Reactive or Inflammatory Lymphadenitis
43
The most important leukocytes capable of phagocytosis
Neutrophils
Macrophages
44
The journey of leukocytes from the vessel lumen to the tissue is mediated and controlled by
Chemokines
45
Phases of the leukocyte journey to the tissue that occur in the lumen
Margination
Rolling
Adhesion to endothelium
46
Cytokines are secreted by ……………………. in tissues in response to microbes and other injurious agents
Sentinel cells
47
L selectin is expressed on
Leukocytes
48
E selectin is expressed on
Endothelium
49
P selectin is expressed on only endothelium T/F
F. Expressed on both platelets and endothelium
50
Ligands for selections are
Sialylated Oligosaccharides bound to mucin-like glycoprotein backbones
51
The expression of selectins and their ligands is regulated by
Cytokines
52
What cytokines induce the coordinate expression of numerous adhesion molecules
TNF
IL-1
53
What stimulates the redistribution of P selectin from the Weibel Palade bodies
1. Histamine and Thrombin
54
Firm adhesion is mediated by a family of heterodimeric leukocyte surface proteins called
Integrins
55
B1 integrin, VLA-4 is to
VCAM 1 (Vascular cell adhesion molecule 1)
56
B2 integrins, LFA 1 and Mac 1 are to
ICAM 1 (intercellular adhesion molecule 1)
57
Leukocytes normally express integrins in what state
Low affinity state
58
Chemokines produced at the site of the injury bind to
Endothelial cell proteoglycans
59
Chemokines bind to leukocytes and activate
rolling leukocytes
60
Chemokines activate the conversion of VLA-4 and LFA1 integrins on the leukocytes to what state
High affinity state
61
The migration of the leukocytes through the endothelium is called
Transmigration or Diapedesis
62
Transmigration of leukocytes occurs mainly in
Post capillary venules
63
Molecules between endothelial cells involved in the migration of leukocytes are
CD31 or PECAM 1(Platelet endothelial cell adhesion molecule)
64
Only exogenous substances can act as chemoattractants T/F
F. Exogenous and endogenous substances can act as chemoattractants
65
The most common exogenous chemoattractants are
Bacterial products
Some lipids
66
Endogenous chemoattractants include:
1. IL-8 (cytokines)
2. C5a (components of the complement system)
3. LTB4 (arachidonic acid metabolites)
67
Chemotactic agents bind to specific ……… on the surface of leukocytes
7 trans membrane GPCRs
68
Signals from the leukocyte GPCRs activate second messengers that (2)
1. Increase cytosolic calcium
2. Activate small GTPs of the Rac/Rho/cdc42 family
69
Leukocyte surface signals induce
1. Polymerization of actin at the leading edge of the cell
2. Localization of MYOSIN filaments at the back
70
In most forms of AI, neutrophils predominate the inflammatory infiltrate during
The first 6 to 24hours
(Replaced by monocytes in the next 24 to 48 hours)
71
What cells become the dominant population in prolonged inflammatory reactions
Monocytes
72
In what situation is the cellular infiltrate dominated by continuously recruited neutrophils for several days?
Pseudomonas bacteria
73
In viral infections, what cells are the first to arrive
Lymphocytes
74
Hypersensitivity reactions are dominated by
Lymphocytes
Macrophages
Plasma cells
75
What’s the dominant population of the cellular infiltrate in allergic reactions
Eosinophils
76
Agents that block ………… are among the most successful developed therapeutics for Chronic Inflammatory Do
TNF
77
Recognition of what cells induces leukocyte activation for clearance
Microbes or Dead cells
78
In phagocytosis and clearance, Leukocyte activation results in
1. Increases in cytosolic Ca2+
2. Activation of enzymes (pkC, PLA2)
79
What are the Three steps in Phagocytosis
Recognition and Attachment
Engulfment
Killing or Degradation
80
Examples of phagocytic receptors
Mannose receptors
Scavenger receptors
Receptors for various opsonins
81
The ……………. receptor recognizes microbes and not host cells
Mannose
82
Mac 1 may also bind microbes for phagocytosis T/F
T
83
The major opsonins are
1. IgG antibodies
2. the C3b breakdown product of complement
3. Certain plasma lectins (mannose-binding lectin)
84
Extensions of the cytoplasm used for engulfment
Pseudopods
85
Vesicle that encloses foreign particle
Phagosome
86
Phagocytosis is dependent on
Polymerization of actin filaments
87
Killing of microbes is accomplished by
Reactive Oxygen species
Reactive Nitrogen species
Lysosomal enzymes
