6. Innate Immunity: Inflammation & Wound Healing Flashcards
(94 cards)
1
Q
Lines of defense (3)
A
- 1st: innate (natura/native) immunity - 2nd: inflammation - 3rd: adaptive (acquired) immunity
2
Q
What 3 things are part of innate immunity?
A
- physical barriers - epithelial cell-derived chemicals - normal microbiome
3
Q
What organ systems are lined w/ physical barriers?
A
the GI, genitourinary, and respiratory tracts
4
Q
List 5 chemical barriers that are part of the innate immune system
A
- saliva - tears - ear wax - sweat - mucus
5
Q
What major problem can occur to the skin? What problems will this cause?
A
skin burns -> cause problems w/ infection and hydration
6
Q
What can happen if you lose your normal microbiome? List 2 examples.
A
other bacteria can overgrow; yeast in the vagina and clostridium deficile in the intestines (pseudomembranous colitis)
7
Q
What is the treatment for Cdiff?
A
Oral flagyl and vancomycin or stool transplant if antibiotics don’t work
8
Q
List 4 characteristics of the inflammatory response
A
- occurs in vascularized tissues - activates rapidly (in seconds) after damage occurs - depends on activity of both cellular and chemical components - nonspecific
9
Q
At the beginning of the inflammatory reaction, what are 3 vascular responses that occur?
A
- vasodilation - increased vascular permeability - WBC adherence to the inner walls of vessels and migration through vessels
10
Q
List 4 goals of inflammation
A
- limit and control inflammatory process - prevent/limit infection and further damage - initiate adaptive immune response - initiate healing
11
Q
What causes edema at the site of injury?
A
increased vascular permeability -> plasma proteins leak from capillary bed -> oncotic pressure -> fluid will follow protein out of capillary -> edema
12
Q
Who are the 1st and 2nd responders at a site of inflammation?
A
1st responder: neutrophil 2nd responder: macrophage (from monocyte)
13
Q
What 3 things occur in response to cellular injury and/or pathogenic invasion (infection)?
A
- mast cell degranulation - activation of plasma systems - release of cellular products
14
Q
List the 3 plasma systems
A
- complement - clotting - kinin
15
Q
Symptoms of acute inflammatory response and causes?
A
- vasodilation (erythema/warmth) - vascular permeability (edema) - cellular infiltration (pus) - thrombosis (clots) -> helps encapsulate bacteria - stimulation of nerve endings by kinin (pain)
16
Q
cells filled w/ granules and located in loose connective tissue close to blood vessels
A
mast cells
17
Q
2 ways mast cells release chemicals
A
degranulation (immediate) and synthesis (delayed)
18
Q
What 3 types of granules are released by mast cells?
A
- histamine - chemotactic factor for neutrophils - chemotactic factor for eosinophils
19
Q
List 3 mediators synthesized by mast cells
A
- platelet activating factor (PAF) - prostaglandins - leukotrienes
20
Q
Function of PAF
A
platelet activation and vasodilation
21
Q
Function of prostaglandins
A
increased vascular permeability, neutrophil chemotaxis, and pain
22
Q
Function of leukotrienes
A
smooth muscle contraction, increased vascular permeability
23
Q
Ex. of leukotriene inhibitor
A
Singulair
24
Q
Ex. of prostaglandin inhibitor (inhibits enzyme for production)
A
Ibuprofen
25
Explain histamine's function after being released from mast cells
vasoactive: temporary rapid constriction of large blood vessels and dilation of post-capillary venues; retraction of endothelial cells lining capillaries (junctions)
26
Which receptor is pro- inflammatory and anti-inflammatory for histamine?
H1 - pro H2 - anti
27
Where are H2 receptors abundant and what will activating them cause?
parietal cells of gastric mucosa -\> activation via histamine will cause secretion of gastric acid
28
Explain the compliment system
- C3 -\> C3b + C3a - C3b -\> C5 -\> C5b + C5a - C5b -\> C6-9 -\> membrane attack complex - MAC forms pores in pathogen membrane to damage it
29
What in the compliment system creates opsonin? What is the function of opsonin?
- C3b - coats surface of bacteria and increases their susceptibility to phagocytosis
30
potent anaphylatoxin in the compliment system -\> mass cell release of histamine
C3a
31
Anaphylatoxin and chemotactic factor in compliment system -\> leukocyte (neutrophil) migration
C5a
32
main protein in a blood clot
fibrin
33
3 functions of clots
- plug damaged vessels and stop bleeding - trap microorganisms and prevent spread to other tissues - provide framework for future repair/healing
34
What activates the extrinsic pathway of the clotting system?
tissue factor (TF) - released by damaged endothelial cells in blood vessels (external trauma)
35
What activates the internal pathway of the clotting system?
activated when the vessel wall is damaged (trauma inside the blood vessels)
36
- Factor unique to extrinsic pathway - Factor unique to intrinsic pathway - Factor activated by both pathways
- Extrinsic: VIIa - Intrinsic: XII (Hageman Factor) -\> XIIa - Both: Xa
37
Describe the common pathway of the clotting cascade
Xa -\> thrombin -\> fibrinogen -\> fibrin -\> blood clot
38
functions to activate and assist inflammatory cells; interacts closely w/ coagulation system
Kinin system
39
Primary kinin
bradykinin
40
What activates the kinin system?
activation of Hageman factor (XII) to XIIa (aka prekallikrein)
41
Functions of bradykinin
- vasodilation (like histamine) - induce pain (w/ prostaglandins) - smooth muscle contraction - increase vascular permeability - leukocyte chemotaxis
42
Cytokines that cause vasodilation (3)
- prostaglandins - histamine - NO
43
Cytokines that cause vascular permeability (4)
- histamine - bradykinin - leukotrienes - PAF
44
Cytokines that cause pain (2)
- prostaglandins - bradykinin
45
Cytokines that cause fever (4)
- IL-1 - IL-6 - TNF-a - prostaglandins
46
Cytokines that activate leukocytes (2)
- IL-1 - TNF-a
47
Cytokines that activate mast cells and eosinophils (2)
- IL-4 - IL-5
48
List acute phase reactants (5)
IL-1, IL-6, IL-8, TNF-a, and C-reactive protein
49
What does C-reactive protein tell about inflammation
global test for inflammation (doesn't tell cause or location; only that it exists)
50
Normal WBC count
5,000-10,000
51
increased neutrophils?
acute bacteria/acute inflammation
52
increased lymphocytes?
vital infection/chronic bacterial infection
53
increased monocytes?
inflammation
54
increased basophils?
allergic reaction
55
increased eosinophils?
parasitic infection
56
3 types of granulocytes
- basophils - eosinophils - neutrophils
57
type of innate lymphocyte
natural killer cell (NK cell)
58
5 types of WBC found on differential
- lymphocyte - monocyte - neutrophil - basophil - eosinophil
59
How do cytokines limit inflammation?
- inhibit production - inhibit macrophage proliferation - destroy histamine and leukotrienes
60
How do cytokines help w/ repair and healing?
- activate macrophages - stimulate fibroblast growth - stimulate endothelial growth
61
Explain VEGF function and how it relates to cancer and chemo
- VEGF is angiogenic -\> vascular growth - found in some cancers to help them develop blood supply - some chemo targets this -\> will also delay healing
62
What does the erythrocyte sedimentation rate test?
how fast RBCs settle at the bottom of the test tube -\> faster may mean inflammation
63
How do cytokines help w/ phagocytosis?
- adherence and diapedesis - chemotaxis - opsonins - activate and increase macrophages
64
Type I interferons (IFN)
INF-a and INF-b
65
What causes production of type I interferons? What do these IFNs do?
produced and released by virally infected cells in response to double stranded RNA -\> induce production of antiviral proteins
66
Type II interferon (IFN)
IFN-y
67
What produces INF-y and what does IFN-y do in response?
produced primarily by lymphocytes -\> activates macrophages -\> increased killing activity by macrophages
68
What produces interleukins (IL)?
primarily macrophages and lymphocytes in response to a pathogen or stimulation by other cytokines
69
IL that is pro inflammatory an endogenous pyrogen (causes fever)
IL-1
70
IL that directly induces hepatocytes to produce proteins needed for inflammation and stimulate differentiation and growth of BM cells
IL-6
71
List 3 systemic effects of TNF-a
- induces fever (endogenous pyrogen) - increased synthesis of inflammation proteins by liver - muscle wasting (cachexia) and intravascular thrombosis in cases of severe infection/cancer
72
What IL is anti-inflammatory?
IL-10
73
What cells secrete TNF-a?
macrophages
74
attract leukocytes to site of inflammation?
chemokines
75
What activates platelets and what does their activation lead to?
activated by tissue destruction/inflammation -\> leads to interaction w/ clotting cascade
76
macrophages that predominate in early inflammation and become a component of purulent exudate
neutrophils (PMNs)
77
Life cycle of monocytes
produced in the BM -\> travel to site of inflammation about 24 hours after neutrophils -\> develop into macrophages
78
defense against parasites and regulation of vascular mediators
eosinophils
79
primary phagocytic cells located in the peripheral organs and skin -\> migrate though lymphatics to lymph nodes to interact w/ T cells
Dendritic cells
80
adherence of leukocytes to endothelial cells
margination
81
emigration of cells through endothelial junctions
diapedesis
82
protein filled watery exudate that indicates early inflammation
serous
83
thick, clotted exudate -\> indicates more advanced inflammation
fibrinous
84
pus filled exudate that indicates bacterial infection or inflammation (supperative)
purulent
85
2 types of exudate that indicate bleeding
serosanguinous and sanguinous
86
3 systemic manifestations of acute inflammation
- fever - leukocytosis - increased plasma protein synthesis (ex. CRP, fibrinogen, amyloid etc.)
87
causes of chronic inflammation (5)
- unsuccessful acute inflammation - high lipid/wax content of microorganisms - ability to survive in macrophage - toxins - chemical or physical irritants
88
bacteria circulating in the blood
bacteremia
89
presence and multiplication of bacteria in the blood
septicemia
90
Explain what happens intracellular after phagocytosis
phagosome (carrying microbe) fuses w/ a lysosome (digestive enzymes) -\> creates phagolysosome (kill and digest microbes)
91
Risks that lead to dysfunctional wound healing
- hemorrhage - fibrous adhesion - hypovolemia - lack of nutrients - poor control of glucose levels - infection
92
raised scar from original skin level (4mm above skin)
keloid scar
93
scar that is larger than it should be
hypertrophic
94
Reasons why inflammation is less in older adults
- impaired function phagocytes - impaired inflammation due to chronic illness - chronic medication intake reduces inflammation response
