Inflammation - Key Terms Flashcards
(101 cards)
1
Q
Goals of Inflammation
A
- Eliminate initial cause of injury
- Remove dead cells
- Begin process of tissue repair
2
Q
Innate immunity
A
The defense system a person is born with
3
Q
Components of innate immunity
A
- Physical barriers
- Enzymes (lysozymes)
- Complement proteins
- C-reactive protein
- Toll-like receptors
- Cells releasing inflammatory mediators
- Antimicrobial peptides
- Phagocytes
4
Q
Benefit of inflammation
A
- Interact with acquired immune system
- Prevent further tissue damage
- Prevent spread of infection by dilution of pathogens
- Prepare area for healing
5
Q
Complement proteins
A
Destroy bacteria
6
Q
WBCS
A
Prevent inflammatory response from spreading to healthy tissues, eat pathogens
7
Q
Plasma protein system
A
Clotting
8
Q
Granulomatous response
A
Inflammation contains the infection/damaged site by walling it off
9
Q
Vascular events in inflammation
A
- Arterioles temporarily constrict
- Brief vasoconstriction followed by vasodilation (this lasts)
10
Q
What do damaged cells release
A
Prostaglandins and leukotrienes that cause vasodilation
11
Q
What does vasodilation help with during the vascular events
A
- Slows blood velocity
- Increases blood flow to increase tissue perfusion
- Causes redness and warmth at site
12
Q
What are plasma protein systems known as
A
Cascades
13
Q
Complement system
A
Normally circulate in inactive form and cause
1. Increased vascular permeability and vasodilation
2. Chemotaxis
3. Opsonization
4. Cell killing
14
Q
How is complement protein system triggered?
A
- Activated by IgC or IgM antigen-antibody complexes.
- Lectin pathway - can opsonin for phagocytosis or activate next part of cascade
- Alternative pathway activated as part of innate immune system
15
Q
Coagulation/clotting system is activated by
A
Extrinsic and intrinsic pathway
16
Q
Thrombin
A
Enzyme that proteolytically activates fibrinogen
17
Q
Thrombin is a part of what system
A
Clotting
18
Q
What does the clotting system do
A
Stops bleeding, localizes microorganisms, provides a meshwork for repair and healing.
Prevents spread of infection by bacteria remaining at localized site
19
Q
Factor XII
A
Activates plasma proteins, promotes formation of bradykinin and kallikrien.
20
Q
Kinin System
A
Activates and assists inflammatory cells
21
Q
Bradykinin
A
Most important product of kinin system, like histamine
22
Q
What does bradykinin cause
A
Vascular permeability, vasodilation, smooth muscle contraction in lungs, and pain
23
Q
Kinins
A
Potent vasodilators, regulators of inflammatory process, and involved in pain sensation and growth
24
Q
What does the endothelium do during inflammation
A
Represses receptors that help leukocytes leave the vessel
Retract to allow fluid to pass into tissues
25
What is the most important activator of inflammatory response
Mast cell
26
Mast cell
Initiates inflammation by releasing biochemical mediators
27
Histamine
Major vasoactive amine released from mast cells
28
What does histamine do
Dilation of capillaries and retraction of endothelial cells lining capillaries to increase vascular permeability Causes bronchoconstriction
29
Chemotactic factors
Attract neutrophils and eosinophils to inflammation site
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Neutrophil chemotactic factor
Attracts neutrophils
31
Eosinophil chemotactic factor
Attracts eosinophils
32
What do mast cells release after granules are released
Leukotrienes, prostaglandins, platelet-activating factor
33
Leukotrienes
Slower and more prolonged responses than histamine in later stages
34
Prostaglandins
Similar effects to leukotrienes and also induce pain
35
Platelet-activating factor
Similar effect to leukotrienes and platelet activation - causes blood clotting
36
Chemotaxis
Movement of an organism in response to a chemical stimulant
Causes WBCs to move
37
Leukocyte
White blood cell
38
Phagocytosis
Lysozyme fuse with phagosome and digest it
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Granulocytes
Neutrophils, eosinophils, basophils/mast cells
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Monocytes
Monocytes, macrophages, dendritic cells
41
Lymphocytes
T cells, B cells, Natural killer cells
42
Neutrophils
Most common type of WBC
First responders to injury/inflammation
Live about 5 days
Actively phagocytose bacteria
43
When do monocytes become macrophages
When they enter the site 24 hours after neutrophils and replace them
44
Dendritic cells
Antigen-presenting cells found in tissue that contacts the external environment
45
Natural killer cells
Large, granular lymphocytes activated by T-cell released cytokines
Contain perforin and granzyme
46
Perforin and granzyme
Activate cell apoptosis via cell membrane receptors
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Platelets
Interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation
48
Primary cell types that produce mediators during acute inflammation
Macrophages, dendritic cells, mast cells
49
Mediators produced in response to specific stimuli
Short-lived and stimulate the release of other mediators which amplifies the inflammatory response
50
Serotonin
Stored in platelets and neuroendocrine cells in the GI tract - cause vasconstriction
51
Eicosanoids
Lipid mediators
52
Cytokines
Cells of the innate immune system secrete many biochemical mediators that are responsible for activating other cells.
Small proteins that are pro-inflammatory or anti-inflammatory
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What are examples of cytokines
Interleukins, chemokines, interferons
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Interleukins
Most important proinflammatory cytokines are interleukin 1, 6, and tumor necrosis factor-alpha
55
Interleukins are primarily produced by
Macrophages and lymphocytes
56
IL-6
Stimulates growth and differentiation of blood cells in the bone marrow, induces hepatocytes from the liver to produce acute phase proteins
57
Chemokines
Group of signaling proteins that act as chemoattractants to recruit leukocytes to areas of damaged tissue
58
Interferons
Produced by cells that are infected by viruses
59
Tumor necrosis factor-alpha
Secreted by macrophages in response to PAMP and toll-like receptor recognition.
Induces fever by acting as an endogenous pyrogen.
60
Serous exudate
Fluid accumulation as a result of tissue injury that does not contain many cells. Watery plasma leaks into IF - blister which indicates early infection
61
Exudative
Contains proteins
62
Fibrinous inflammation
Result of large vascular leak that allows fluid with large proteins to leak out into surrounding tissue
Causes thick clotting
63
Purulent inflammation
Forms pus, which contains many neutrophils, cellular debris, and edema fluid.
Usually walled-off lesions with an abscess/necrotic center
64
Suppuration
Formation of pus that may occur if the pathogen is difficult to eliminate or severe
65
Pyogenic bacteria
Commonly causes pus formation
66
Ulceration
Results from very severe inflammation and is a local defect caused by necrosis of cells and sloughing of necrotic tissue
67
Pattern Recognition Receptors (PRR)
Help to identify pathogen-associated molecular patterns, leading to production and release of cytokines and other chemicals that mediate the response of the cells causing inflammation
68
Anti-inflammatory pathways
Hypothalamic-pituitary-adrenal pathway
Sympathetic nervous system
Parasympathetic nervous system
69
HPA anti-inflammatory pathway controls release of
Glucocorticoids - Cortisol
Interleukin-10 inhibits production of proinflammatory cytokines by macrophages
70
Sympathetic nervous system (anti-inflammatory pathway)
Releases NE and epi to downregulate production of pro-inflammatory cytokines and upregulate the production of anti-inflammatory cytokines
Promotes recruitment of leukocytes
Increases blood and lymph flow
71
Parasympathetic nervous system
Inhibits pro-inflammatory cytokine production in the spleen and decreases neutrophil activation
72
Principal systemic effects of inflammation are
Fever and increases in levels of circulating leukocytes and plasma proteins.
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Acute-phase response (definition)
Systemic effects caused by chemical mediators in inflammatory response
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Acute-phase response
Fever, increase in serum proteins, leukocytosis, release interleukins and tumor necrosis factor
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Systemic inflammatory response syndrome (SIRS)
Severe systemic response to inflammation
Cause is infection: sepsis
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Septic shock
Bacterial or fungal - vasodilation - peripheral pooling - decreased BP
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Gut barrier failure
Decrease perfusion of the gut, normal flora bacteria and toxins escape into tissue fluid, inflammatory response, vasodilation, shock
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Multiple organ dysfunction syndrome
Progressive dysfunction of two or more organ systems from uncontrolled inflammatory response to severe illness or injury
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Acute inflammation is characterized by
Brisk onset of relatively short duration
Prominent systemic signs and local responses
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Chronic inflammation is characterized by
High levels of lymphocytes, macrophages, monocytes
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Impaired or excessive inflammation is characterized by
Overexpression of leukocyte adhesion molecules
Production of excessive pro-inflammatory cytokines
Damage to tissues
82
Risks for developing chronic inflammation
Poor blood supply, malnutrition, abnormal neutrophil function, prolonged use of anti-inflammatory medications
83
Granuloma
Body walls off and isolates infection to protect against tissue damage
Epitheliod cell formation
84
Chronic inflammation is associated with
Tissue destruction
Replacement of damaged tissue with fibrous tissue via angiogenesis
85
Alzheimer disease
Beta-amyloid peptide plaques and neurofibrillary tangles in the brain
86
Asthma
Chronic airway inflammation, dysfunction of the airways, tissue remodeling
87
Atherosclerosis
Believed to be chronic inflammatory response of leukocytes to low-density lipoproteins particles in arterial walls
88
What does atherosclerosis involve
1. Involve both innate and acquired immunity systems
2. Leukocytes involved mostly monocytes and macrophages
3. Begins in childhood
89
T2D mechanisms that contribute
Excess levels of glucose and free fatty acids from overnutrition
Adipose tissue growth exceeding vascular supply
90
Inflammaging
Chronic, low grade inflammation associated with aging
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Potential causes of inflammaging
Damaged cells that accumulate with age
Gut's inability to adequately respond to harmful substances produced by microbiota
92
Obesity
Adipose tissue secretes hormones, cytokines, chemokines, growth factors, complementary proteins
Adipose tissue implicated in development and progression of many chronic inflammatory disorders
93
Three phases of wound healing
Hemostasis, inflammatory phase, proliferative/reconstruction phase, remodeling/maturation
94
Factors that affect wound healing
Nutrition, circulation, age
95
Hypovolemia (dysfunctional wound healing)
Can't deliver WBCs to injury site
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Hemorrhage (dysfunctional wound healing)
Large clots and increased exudate are mechanical barriers to O2 diffusion, slows repair
97
Fibrous Adhesion
If fibrin not reabsorbed, it forms adhesions and binds organs together
98
Hypoproteinemia
Impairs fibroblast proliferation
99
Anti-inflammatory steroids
Block macrophages from getting to injury and releasing cytokines
100
Dehiscence
Wound pulls apart at the suture line
101
Impaired (excessive) contraction
Contracture: occurs with burns, decreases ROM
