M1: Acute & Chronic Inflammation Flashcards
0
Q
Cell death
A
Necrosis
1
Q
Protective response to rid the initial cause of cell injury. Complex reactions of both blood vessels and leukocytes.
A
Inflammation
2
Q
Fluid portion of the blood
A
Plasma
3
Q
Body’s principal defenders against foreign invaders
A
Plasma proteins, Circulating leukocytes & Tissue phagocytes “PCT”
4
Q
Protein is primarily synthesized in what organ
A
Liver
5
Q
Triggers the vascular & cellular reaction
A
Soluble factors
6
Q
Blood component, polymorphonuclear cell, responsible for Acute Inflammation.
A
Neutrophil
7
Q
Blood component responsible for Chronic Inflammation
A
Macrophage & Leukocyte
8
Q
Primarily from B Lymphocytes
A
Plasma cells
9
Q
Elimination of offending agent is achieved by
A
Termination of Inflammation
10
Q
Blood component that has a short lifespan in tissues
A
Leukocytes
11
Q
Repair of damage tissue/cell. Example is abrasion of skin.
A
Regeneration
12
Q
Filling of the defect with fibrous tissue
A
Scarring
13
Q
Produce by fibroblast
A
Collagen
14
Q
Hardening of the blood vessels
A
Atherosclerosis
15
Q
Cardinal signs of an Infection
A
Rubor, Tumor, Calor, Dolor & Functio Laesa
16
Q
Cardinal sign: redness
A
Rubor
17
Q
Cardinal sign: pain
A
Dolor
18
Q
Cardinal sign: loss of function
A
Functio Laesa
19
Q
Cardinal sign: heat
A
Calor
20
Q
Cardinal sign: swelling
A
Tumor
21
Q
Rapid host response that serves to deliver leukocytes and plasma proteins. Early onset, involving fluid exudation and polymorphonuclear cell immigration.
A
Acute Inflammation
22
Q
Two main components of Inflammation
A
Vascular wall response & Inflammatory response
23
Q
Later onset and longer duration involving lymphocytes and macrophages, with blood vessels proliferation and fibrosis.
A
Chronic Inflammation
24
Calor is due to
Vascular dilatation
25
Rubor is due to
Vascular dilatation & Congestion
26
Tumor is due to
Increased vascular permeability
27
Dolor is due to
Mediator release
28
Functio laesa is due to
Pain, Edema, Tissue injury or scar
29
Three major components of Acute Inflammation: 1. Alterations in _____________, leading to increased blood flow.
Vascular caliber
30
Three major components of Acute Inflammation: Structural changes in the ________, permitting plasma proteins and leukocytes to leave the circulation to produce inflammatory ________.
Microvasculature. Exudates.
31
Three major components of Acute Inflammation: ___________ from blood vessels and accumulation of the site of injury with activation.
Leukocyte emigration
32
Stimuli for Acute Inflammation
Tissue necrosis, Infection & Microbial toxin "TIM"
33
Detects bacteria
Toll-like Receptors
34
Tissue necrosis is due to
Ischemia
35
Produced by cells deprived of O2 & activates transcription of many genes involved in inflammation
Hif 1A
36
Reactions of Blood Vessels in Acute Inflammation
BV, Leukocytes & Termination "BLT"
37
Pathological term for leaky
Vascular Permeability
38
Is excess fluid in interstitial tissue or body cavities
Edema
39
Is an inflammatory, extravascular fluid with cellular debris and high protein concentration. Specific gravity of 1.020 or more.
Exudate
40
Is excess, extravascular fluid with low protein content. It is essentially an ultrafiltrate of blood plasma resulting from elevated fluid pressures or diminished plasma osmotic forces. Specific gravity of 1.012 or less.
Transudate
41
Is a purulent inflammatory exudate rich in neutrophils and cell debris
Pus
42
Normal fluid exchange in vascular beds depends on an intact
Endothelium
43
Normal fluid exchange are modulated by two opposing factors
Hydrostatic pressure & Plasma colloid osmotic pressure
44
Causes fluid to move into the capillaries
Plasma colloid osmotic pressure
45
Causes fluid to move out of the circulation
Hydrostatic pressure
46
Yellowish & Turbid. Escape of fluid, CHONs & cells from the vascular system into the interstitial tissue or body cavities. Inflammatory edema. Increase protein with cellular materials.
Exudate
47
Increase HP & Decrease OP causing transudate
Edema
48
Clear, less hazy & cloudy. Non inflammatory edema. Decreased protein. Little or non cellular material. An ultrafiltrate plasma.
Transudate
49
One of the earliest manifestations of Acute Inflammation. Increase blood flow. Followed by Increase permeability of the microvasculature.
Vasodilation
50
Mediates Vasodilation
Histamine & Nitric Oxide
51
Lining of a vessel
Endothelium
52
Increases when there is vasodilation
Hydrostatic pressure
53
Combination of vascular dilation and fluid loss leads to
Increased blood viscosity & concentration of RBCs
54
Slow movement of erythrocytes
Stasis
55
Vascular congestion
Erythema
56
Increased Vascular Permeability: _________ of venule endothelium to form intercellular ______.
Contraction. Gaps.
57
Contraction of venule endothelium is due to these chemical mediators
Histamine, Bradykinin & Leukotrienes "HBL"
58
Contraction of venules/endothelial cells that occur rapidly after injury and is recersible transient. 15-30mins.
Immediate-transient response
59
Increased Vascular Permeability: Direct _______ injury.
Endothelial
60
Causes endothelial cell necrosis and detachment that affects venules, capillaries and arterioles
Sever necrotizing injury
61
Recruited neutrophils may contribute to the injury through
Reactive Oxygen Species "ROS"
62
Seen in late appearing sunburn
Prolonged delayed response
63
Inflammation of the lymphatics. Secondary inflamed. Red streaks.
Lymphangitis
64
Inflammation of the lymph nodes. Draining LN. Enlarged & painful lymph nodes. May be due to lymphoid follicle and sinusoidal phagocyte hyperplasia.
Lymphadenitis
66
Increased Vascular Permeability: Increased ________.
Transcytosis
67
Transendothelial channels form by interconnection of vesicles derived from the
Vesiculovacuolar organelle
68
Induce vascular leakage by increasing the increasing the number of these channels
Vascular Endothelial Growth Factor (VEGF)
69
Increased Vascular Permeability: _______ from new blood vessels.
Leakage
70
Endothelial proliferation and capillary sprouting result in leaky vessels
Angiogenesis
71
Represent a secondary line of defense when local inflammatory responses cannot contain an infection
Mononuclear Phagocyte System
73
Increased transport of fluids & proteins
Transcytosis
74
In Acute Inflammation, this predominates during the first 6-24 hours.
Neutrophil
75
In Acute Inflammation, this replaces the neutrophil after 24-48 hours.
Monocyte
76
Journey of Leukocytes from the vessel lumen to the interstitial tissue.
Extravasation
77
Extravasation Steps: in the lumen; _________, _________ & __________ to endothelium.
Margination, Rolling & Adhesion
78
Extravasation Steps: Migration; ________ & ________.
Endothelium & Vessel wall
79
Extravasation Steps: Tissue toward a ________ stimulus.
Chemotactic
80
Process of leukocytes redistribution peripheral position of leukocytes along the endothelial surface.
Margination
81
Individual & then rows of leukocytes adhere transiently to the endothelium.
Rolling
82
A chemical mediator that induces expression. Trigger adhesion molecules.
Cytokines
83
Examples of Cytokines
TNF, IL-1 & Chemokines "TIC"
84
These are adhesion molecules which mediates initial rolling
Selectins
85
Found at the surface. Mediates firm adhesion which is commonly seen in neutrophil.
Integrins
86
Induce endothelial expression of Ligands
TNF & IL-1
87
Ligand of endothelial cells for VLA-4 & B1 Integrins
VCAM
88
Ligand of endothelial cells for LFA & B2 Integrins
ICAM
89
Express Integrin in low affinity state
Leukocyte
90
Firm adhesion of Leukocytes to adhesion molecules which then activate & bind to rolling leukocyte. An example is Cytokine.
Chemokines
91
Transmigration
Diapedesis
92
Diapedesis is mediated by
PECAM-1 (Elastase)
93
Pierce the basement membrane by secreting collagenase
Leukocytes
94
Epithelial lining of Endothelium
Simple squamous epithelial cells
95
Directs specific binding location. Locomotion oriented along a chemical gradient. Both exogenous & endogenous substances can act as chemoattractants.
Chemotaxis
96
Leukocyte responsible for viral infection
Lymphocytes
97
Leukocyte responsible for hypersensitivity
Eosinophil
98
Responsible for Antibody production
Plasma cell
99
Source of cytokines
Macrophages
100
Recognizes components of microorganisms
TLRs
101
Recognize short bacterial peptides. Activation of respiratory burst.
G-protein coupled receptors
102
Process of coating a microbe to target it for ingestion which makes it easier to engulf microorganisms.
Opsonization
103
Major macrophage activating cytokine. Secreted by natural killer cells reacting to microbes & by antigen activated T lymphocyte.
Interferon-Ÿ
104
Coats the microbes. IgG antibodies. Mannan-binding lectin & C3B complement Proteins.
Opsonins
105
Steps in Phagocytosis
Recognition, Engulfment & Degradation/Killing "RED"
106
Extension of the cytoplasm
Pseudopods
107
Encloses the particle
Phagosome
108
Phagosome fuses with a lysosomal granule
Phagolysosome
109
Killing & Degradation is done by
ROS
110
Converts H2O2 to hypochloride which a potent antimicrobial agent
MPO in presence of Halide
111
Most efficient bacteriocidal system of neutrophils
H2O2-MPO-Halide
112
Converted to Hydroxyl radical which is another powerful destructive agent
H2O2
113
Produced from Arginine which is for microbial killing
Nitric Oxide
114
Free harmful radical
Peroxynitrite
115
OCl stands for
Hypochlorite
116
ONOO stands for
Peroxynitrite
117
O2' stands for
Superoxide Anion
118
Defects in phagolysosome function
Chedial Higashi Syndrome
119
Defects in microbicidal activity & in genes encoding components of phagocyte oxidase
Chronic Granulomatous Disease
120
Acquired deficiencies due to radiation & chemotherapy
Bone marrow suppression
121
From mast cell, basophil & platelets. Causes dilation of arterioles a d increases the permeability of venules.
Vasoactive Amine: Histamine
122
Stimulates when platelets aggregate after contact with collagen, thrombin, adenosine diphosphate and antigen-antibody complexes.
Serotonin
123
Main source of serotonin
Platelets
124
Exposed when there is blood vessel injury
Subendothelial collagen
125
Converts fibrinogen to fibrin
Thrombin
126
Examples of Arachidonic Acid metabolites
Prostaglandin, Leukotrienes & Lipoxins "PLL"
127
Endothelium-derived relaxing factor. Endogenous mechanism for controlling inflammatory response.
Nitric Oxide
128
C3A & C5A are examples of
Anaphylatoxins
129
Deposition of Collagen
Fibrosis
130
Morphologic Patterns of AI: ________ of small blood vessels.
Dilatation
131
Morphologic Patterns of AI: _________ of blood flow.
Slowing
132
Morphologic Patterns of AI: Accumulation of _______ & _______ in the extravascular tissue.
Leukocytes & Fluid
133
Marked by outpouring of thin fluid derived from plasma or secretions of mesothelial cells
Serous Inflammation
134
Other term for Thin fluid
Effusion
135
From a 2nd degree burn or viral infection
Skin blisters
136
Development of exudate in large vascular leaks. Inflammation in the lining of body cavities. May be removed by __________.
Fibrinous Inflammation. Fibrinolysis.
137
Production of pus consisting neutrophils, liquefactive necrosis and edema fluid.
Suppurative/Purulent Inflammation
138
Pyogenic bacteria is due to what microorganism
Staph
139
Localized collections of purulent inflammatory tissue caused by suppuration in a tissue, organ or a confined space.
Abscess
140
Local defect or excavation of the surface an organ or tissue that is sloughing.
Ulcers
