Inflammation Flashcards
1
Q
acute inflammation is a response to
A
recent injury or infection
2
Q
what is acute inflammation characterized by?
A
vasodilation
increased capillary permeability
neutrophils are main players
3
Q
what is chronic inflammation a response to?
A
variable response to ongoing injury or infection
4
Q
what is chronic inflammation orchestrated by?
A
t-helper cells
t-cells, b-cells, macrophages, eosinophils, fibroblasts may be involved
5
Q
is inflammation infection? Immunity?
A
inflammation is not infection or immunity
6
Q
what did Celsus describe?
A
manifestations of inflammation
-redness, heat, mass, pain
7
Q
what did Virchow do?
A
added a fifth manifestation of inflammation
-loss of function
8
Q
triple response of Lewis
A
red scratch
flare around scratch
swollen area around flare
1 & 3 mediated by histamine, 2 by autonomics
9
Q
hallmarks of acute inflammation
A
vasodilation
increased capillary permeability
neutrophil infiltration
10
Q
vasodilation-1
A
increased blood flow-redness and heat
11
Q
increased capillary premeability-2
A
leakage of fluid and proteins
osmotic water loss-swelling
leakage of fibronigen leads to clotting
12
Q
neutrophil infiltration-3
A
margination, emigration, chemotaxis
phagocytosis & degranulation-pain
monocytes/macrophages appear later
13
Q
margination
A
neutrophils adhere to capillary walls
14
Q
emigration (diapedesis)
A
neutrophils pass through capillary walls
15
Q
chemotaxis
A
neutrophils follow chemical signals to damage/infection
16
Q
phagocytosis
A
neutrophils engulf pathogens and debris
17
Q
degranulation
A
neutrophils release cytoplasmic granules
18
Q
what is due to histamine?
A
vasodilation and capillary permeability
19
Q
what does margination depend on?
A
neutrophil and endothelial “adhesion molecules”
20
Q
what drives diapedesis and chemotaxis?
A
C5a and various leukotrienes
21
Q
what does phagocytosis rely on
A
opsonins IgG and C3b
22
Q
what does degranulation release?
A
prostaglandins
leukotrienes
free radicals
lysosomal enzymes
23
Q
what interferes with many aspects of neutrophil function?
A
steroids and diabetes
24
Q
leukotrienes
A
act as chemotaxins
25
opsonins
enhance phagocytosis, make bacteria desirable to neutrophils
26
frustrated phagocytosis
lysosomes become extracellular when neutrophil can't eat bacteria, spills out into cytoplasm
27
inflammatory mediators
chemicals responsible for aspects of inflammation
28
histamine
released from tissue mast cells during injury or infection
| vasodilation & capillary permeability
29
bradykinin
formed from kinin system
vasodilation and capillary permeability
causes pain (bee venom)
30
complement system
collection of plasma proteins that under certain circumstances react with each other in a chain reaction-cascade
31
types of cascades
classical and alternate
32
classical and alternate cascades
two different chain reactions that ultimately lead to the same thing
33
C3a/C5a
stimulate mast cells to release histamine
34
what happens when you have an exaggerated amount of histamine?
you can go into anaphylaxis
35
C5a
acts as perfume, chemotaxin
36
C3b
opsonin, enhances phagocytosis
37
what is the end result of the complement system cascade-classical and alternate?
collection of complement proteins C5-C9 combine together to form membrane attack complex, punches holes in membranes
38
arachidonic acid metabolites
phospholipase A2 liberates AA from cell membranes
39
what is phospholipase A2 inhibited by?
steroids
40
cyclooxygenase
converts AA into prostaglandins
41
what inhibits cyclooxygenase?
aspirin and NSAIDs
42
5-lipoxygenase
converts AA into leukotrienes
43
what does cyclooxygenase produce?
prostaglandins
44
list prostaglandins
| produced by cyclooxygenase
thromboxane A2
Prostacyclin (PGl2)
Prostaglandin E2
45
thromboxane A2
produced by platelets
| vasoconstriction, platelet aggression
46
prostacyclin PGl2
produced by endothelial cells
| vasodilation, prevents platelet aggression
47
prostaglandin E2
vasodilation, potentiates bradykinin(pain), fever
48
what does lipoxygenase produce?
leukotrienes
49
list leukotrienes
| produced by lipoxygenase
leukotriene C4
| leukotriene B4
50
leukotriene C4
increased capillary permeability
breaks down to LTD4 and LTE4
each causes smooth muscle constriction
51
leukotriene B4
neutrophil and monocyte chemotaxis
52
monokines
released from monocytes/macrophages
| produce acute phase reaction
53
what are included in acute phase reaction?
interleukin-1 and tumor necrosis factor alpha (cachectin, TNF-a)
54
acute phase reaction
"sick" from inflammatory illness
shift in hepatic protein synthesis, more complement, clotting, c-reactive protein
-increased erythrocyte sedimentation rate ("sed rate")
55
sed rate
nonspecific marker for course of inflammation
56
c-reactive protein
risk factor for coronary disease
57
what does SIRS stand for?
systemic inflammatory response syndrome
58
what is SIRS?
exuberant production of inflammatory mediators
59
what does SIRS result in?
multisystem organ failure due to normal tissue damage
60
who is affected by SIRS?
super sick people in ICU
61
what is the outcome of acute inflammation where neutrophils win?
complete resolution with no tissue damage
62
what is the outcome of acute inflammation where neutrophils win but there are civilian casualties?
healing by scarring
63
what is the outcome of acute inflammation where neutrophils cannot destroy but wall off?
abscess formation-"put" in a confined space other than a body cavity
64
what is the outcome of acute inflammation where neutrophils and mediators cannot remove the noxious agent?
progression to chronic inflammation
65
what is chronic inflammation defined as?
infiltration of mononuclear cells
| -monocytes, lymphocytes, plasma cells
66
does chronic inflammation include immune?
some crossover into immune system activation may be present
67
what can chronic inflammation produce?
granulomas-macrophages adhere to each other and wall off stuff
68
granulomatus diseases/disorders
foreign bodies
tuberculosis
deep fungal infections
sarcoidosis
69
what is the predominant cell in infections by common bacteria (staph, strep, gram-negative rods)?
neutrophil
70
what is the predominant cell in spirochete diseases (syphilis and Lyme)?
plasma cell
71
what is the predominant cell in tuberculosis and fungal infections?
monocyte/macrophage
72
what is the predominant cell in infections caused by worms?
eosinophil
73
how could there be no inflammatory reaction?
depending on agent and host
| example-diabetic on steroids
74
what are the 2 courses following inflammation for damaged tissue?
regeneration of functional cells
| repair by fibrous tissue ("scar")
75
labile cells
continuous replicators
| ex. epithelium
76
stable cells
discontinuous replicators
don't normally regenerate but have capacity
glandular cells, fibroblasts, endothelium, osteoblasts, liver regeneration
77
permanent cells
non-replicators
| glia, neurons, heart
78
repair-does damaged epithelium keep free edge?
No, cannot tolerate.
| rapid re-epithelization by regeneration
79
what replaces damaged cells?
connective tissue replaces permanent cells
80
how does connective tissue replace permanent cells?
fibroblasts proliferate
-produce ground substance & collagen fibers
endothelial cells proliferate
-form new, leaky vessels
both invade and eventually displace the clot
81
what is an immature scar?
granulation tissue
82
what happens in maturing scars?
enough collagen to fill the void
re-epithelization completes
type III collagen replaced by type I
fibroblasts contract & return to rest
Most new vessels resorb
Never attains strength of original tissue
83
what is the ideal situation for wound healing?
primary intention
84
what does a surgical would healing by primary intention look like?
little necrosis
no infection (hopefully)
edges approximated
85
primary intention: minutes
clotting cascade activated, stops the bleeding
86
primary intention: 24 hours
neutrophils enter, epithelial cells are regenerating from the edges
87
primary intention: 3 days
macrophages enter, granulation tissue appears, epithelial cells now cover the wound surface
88
primary intention: 5 days
granulation tissue fills the entire wound
89
primary intention: 2 weeks
fibroblasts multiply, collagen accumulates
90
primary intention: 4 weeks
overlying epidermis complete sans adnexal structures, capillary involution & scar contraction occurring, red scar turns white
91
what does secondary intention mean?
wound that can't be closed or won't be due to high risk of infection, heavily contaminated
92
what does secondary intention look like?
no approximation
93
what happens in secondary intention?
larger fibrin meshwork (scab), more inflammation, possibly infection, more granulation tissue, spectactular wound contraction
94
what happens after complete re-epithelization in secondary intention?
scab is pushed off
95
how long does it take for secondary intention to heal?
much longer than primary intention
96
what does secondary intention produce?
always a deformity
97
contracture
fibroblasts contract too much, can be crippling
98
what causes contracture?
burns, ugly surgery
99
hypertrophic scar
exuberant scar tissue formation
100
does hypertrophic scar go beyond wound margins?
no, stays within wound margins
101
does hypertrophic scar regress?
yes
102
keloids
exuberant scar tissue formation
103
do keloids go beyond wound margins?
yes, usually enlarge
104
hindrances to adequate healing
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NOT OLD AGE
inadequate nutrition-protein, vitamin C, zinc
poor blood supply
foreign bodies
infection
glucocorticoid (steroid) therapy
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