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inflammation Flashcards

1
Q

signs and symptoms of inflammation

A
  • Heat (calor)
  • redness (rubor)
  • swelling (tumor)
    =all due to vascular changes
  • pain (dolar)
    -loss of function due to chem mediators and leukocytes
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2
Q

length of acute inflammation

A

hours to days

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3
Q

what is the characteristis of accute inflammation

A

exudation

neurtrophil infiltration

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4
Q

length of chronic inflammation

A

days-years

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5
Q

characteristics of chronic inflammation

A
  • mononuclear inflammatory cell (lymphocytes, macrophages, plasma cells)
  • infiltration with vascular proliferation
  • fibrosis later
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6
Q

does chronic or accute inflammation cuase additional tissue damage

A

both

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7
Q

what mediates a fever

A

IL-1, TNF, PGE2

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8
Q

what happens to blood flow during acute inflmmation

A

Increased vascular permeability

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9
Q

what does the change in microvasculature do in acute inflammation

A

promote fluid (edema) and inflammatory cell accumulation in the tissue at the site of injury

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10
Q

where does vasodilation begin in acute inflammation

A

in the precapillary arterioles

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11
Q

what does vasodilation account for in acute inflammation

A

redness and heat

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12
Q

what mediates vasodilation in accute injury

A

NO from endo cells
Histamine from mast cells
maintained by prostaglandins

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13
Q

what does increased vascular permeability lead to

A
  • movement of fluid out of the microvasculature (transudate or exudeate)
  • blood concentrates and slows (statis)
  • movement of inflammatory cells out of vessels (Diapedesis) occurs at post-capillary venules
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14
Q

what leads to swelling in acute injury

A

Accumulation of fluid in the extravascular tissue (Edema)

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15
Q

what is the physical characterists of transudate

A

Low protein
Low specific gravity
clear and yellow

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16
Q

what is non inflammatory transudate casued by

A

Endothelium still intact

fluid accumation due to increased hydrostatic pressure or decreased serum oncotic pressure

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17
Q

what causes inflammatory transudate

A

early endothelial cell conctration

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18
Q

is transudate or exudate for tissue and endothelial cell damage

A

Exudate

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19
Q

what makes up exudate

A

high protein contenet
high specific gravity
contains inflammatory cells usually

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20
Q

chacteristics of fibrinous exudate

A

High protein (fibron)
Few cells
Cloudy

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21
Q

chacteristis of Purulent exudate

A

Also called pus
Contains cells (neutrophils
Opaque

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22
Q

characters of Sanguineous exudate

A

Pink and red fluid due to fluid

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23
Q

where does Fibrinous exudate occur

A

around body organs

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24
Q

what causes purulent exudate

A

BActerial

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25
what causes Sanguineous exudate
Break down in the blood barrier
26
what may cause increased vascular permeability during inflammation
``` Endothelial contraction Endothelial retration =due to mediators Direct injury (non-lethal injury, necrosis or detachment) ```
27
time frame of endothelial contraction in inflammation
Immediate then goes away
28
time frame for endothelial retraction in inflammation
Delayed then can be sustained for 24 hours
29
time frame for direct injury to endothelium in inlammation
Immediate or delayed and is often sustained
30
where does endothelial contraction often occur
post capilary venules
31
what mediates endothelial cell contraction
Histamine bradykinin early, later by leukotrienes and PAF C3a and C5a induce vasoactive amine release that leads to edema
32
what causes endothelial cell retraction
Restructuring of the cytoskeletal proteins
33
what mediates Endothelial cell retratction
IL-1 TNF IFN-gamma
34
what may causes direct venule endothelial injury
Neutrophilic release of reactive ocygen species and lysosomal enzymes (proteases) during inflammation
35
what factors mediate pain
Bradykinin | PGE2
36
what factors mediate fever inflammation
IL-1 TNF PGE2
37
what facotrs activate endothelail cells in inflammation
``` Histamine Thrombin Complement factors Cytokines - IL-1 and TND Bacterial production Hypoxia VIruses PAF ```
38
what do activated endothelail cells produce and why
PGI2 and NO to induce vasodilation
39
do endotheial cells contract of dilate during inflammation
Contract
40
what oes the cytoskelton of endothelial cells do during inflammation
Rearrange to retract
41
what does the surface of endothelial cells due during inflammation
INcrease expression and affininty of surface cell adhesion molecules
42
what does acitvated endothelial cells produce during inflammation
synth and release Inflammatory mediators - PGI2 - PAF - IL-1 - IL-6 - Chemokines
43
hoe does Leukocyte etravasation occure (Steps
``` Leukocyte margination Leukocyte rolling Leukocyte adhesion Emigration Chemotaxis ```
44
what leads to margination of leukocyte
Physical forces often due to stasis
45
what leads to rolling of leukocytes
Selectins (weak, transient, sticking)
46
what leads to adhesion of leukocytes
Integrins (ICAM, VCAM)
47
what causes emigration of leukocytes
PECAM
48
what do chemotactic factors do besides points cells to go in certain direction
stimulate leukocyte activation
49
what are the chemotactic factors for leukocyte extravasion
``` PAF (potent) LTB4 (Potent) C5a Chemokines Bacterial lipids and peptides Fibrin Degradation products (FDP) ```
50
what activates Leukocytes in an inflammatory response
``` Bacterial products Cellular debris Ab-Ag complexes Cytokines and chemokines CHemotactic factor ```
51
what does a leukocyte produce when activated
- Leukotrienes and prostaglandins from arachidonic acid - ROS - Cytokines
52
what does a leukocyte releases when acivated
Degradulation and release of lysosomal enzyme
53
what happens to the cell adhesion molecules when leukocytes are activated
Altered expression of cell adhesion molecules
54
How does A leukocyte do phagocytosis
Attachement Engulfment into a phagocytic vacuole Lysosomal degranulation by fusion with the phagosome Oxidate burst releasing ROS Other mech of intracellular killing: lysozyme, major basic protein, defensins, bactericidal permeability-increasin gprotein
55
what allows for Leukocyte attachment during phagocytosis
mediated by opsonins (IgG, C3b, collectins) on targets and specific leukocyte receptors (Fc receptor for IgG, complement receptors)
56
what enzyme is responsible for creating NO
iNOS from arginine
57
cells of ACute inflammation
Neutrophils | Monocytes (macrophages/histiocytes)
58
what is the morphologic hallmark of acute inflammation
NEutrophils
59
when do neutrophils begin to accumulate
within 6-24 hours after accute injury
60
why do NEutrophils infiltrate tissue
In response to tissue necrosis, bacterial, and some fungal infection
61
what does a neutrophil do after phagocytosis and digestion
Undergoes apoptosis and phagocytosis
62
why does a neutrophil undergo apoptosis after phagocytosis and digestion
Release ROS and lysosomal enzymes
63
when do monocytes come in
after Neutrophils, begining 48 hours inflammation
64
when do monocytes become histiocytes or macrophages
after entering into a tissue
65
how long are monocytes present during inflammation
last months (circulating monocytes only last a day)
66
functions of activated macrophages
Phagocytize and digest cellular debris and organ take up antigens and present to immunocompetent T cells Elaborate various factors
67
what are the various factors monocytes elaborate upon activation
``` Enzymes (proteases) Complement and Coagulation factors Cytokines (IL-1, TNF) ROS, and NO Prostaglandins Growth factors for healing and repair ```
68
roll of lymphocytes
Immune function
69
Roll of eosinophils
Allergic reaction, parasites
70
Roll of MAst cels
Release Histamine
71
what are the characteristics of Cellulitis inflammation
Diffuse, permeative infiltration of neutrophils with edema
72
What are the characteristics abscess inflammation
Localized area of liquefactive necrosis
73
what is an ulcer
Erosion of epithelial surface exposing underlying connective tissue
74
what cells are found in acute inflammation
Polymorphonuclear cells (innate)
75
what cells are found in chronic inflammation
lymph and more (addaptive)
76
is accute or chronic inflammation fatal
Both are reversible or fatal
77
Causes of Chronic Inflammation
Persistent Infection prolonged exposure to a toxic agent Immune-mediated inflammatory disease
78
what type of inflamation is often associated with tissue repair
Non-specific chronic inflammation
79
what cells are present for non-specific chronic inflammation
``` Macrophages Lymphocytes Plasma cells Eosinophils FEw neutrophils ```
80
what type of recation granulomatous inflmmation linked to
Delayed type IV hypersensitivity immune reaction (Chronic)
81
what is the Morphology of granulomatous inflammation
Epithelioid (activated) Histiocytes) Central Caseous necrosis often present Epithelioid histiocytes together in a multinucleated giant cells Collar of mononuclear cels
82
what do epithelioid (Activated) histiocytes look like
Granular pink cytoplasms with indistinct cell borders
83
What do older granulomas eventually develop
A rim of fibroblasts and connective tissue
84
how does Granulomatous inflammation heal
Heal by fibrosis
85
what can causes granuloma | tous inflammation
``` BActerial infection Parasitic infection Fungal infection Inorganic matter Unknown ```
86
what bacterial infection can cause granulomatous inflammation
Tuberculosis | Cat scratch fever
87
what parasitic infection can cause granulomatous inflammation
Schistosomiasis | Toxoplasmosis
88
what fungal infection can cause granulomatous inflammation
Coccidioimycosis | Histoplasmosis
89
What inorganic matter can cause granulomatous inflammation
Silicosis | Inert foreign material
90
what are some unkown causes that can cause granulomatous inflammation
Saecoidosis | Crohn's
91
what cells secerete Histamine
Mast cells
92
where does Bradykinin come from
Plasma protein
93
where does NO come from
Endothelial cells + others
94
Where do prostaglandins come from
MEmbrane phospholipids
95
where do leukotrienes C4, D4, E4 come from
Membrane phospholipids
96
where does Leukotriene B4 come from
MEmebrane phospholipids
97
where does PAF come from
Leukocytes | endothelial cells
98
where does IL-1 and TNF come from
Macrophages | Endothelial cells
99
Where does C5a and C3a come from
Plasma protein
100
Roll of Histamine
Vasodilation and increased vascular permeability
101
Roll of bradykinin
increased vascular permeability and pain
102
roll of NO
Vasodilation
103
roll of Prostaglandins
Vasodilation Pain fever Potenetiate other mediators
104
roll of leukotriene C4, D4, and E4
Increase vsacular permeabilty Vasoconstricition Bronchoconstriction
105
Roll of Leukotriene B4
Leykocyte activation | Chemotaxis
106
Roll of PAF
Increaed vascular permeability | Chemotactic
107
Roll of Il-1 and TNF
EC and leukocyte activation Fever Pain
108
Roll of C5a and C3a
Chemotaxis (C5a) Increased Vascular permeability (C3aand C5a) Phagocytosis (C3b)
109
what causes histamine release
Physical injury Ag-IgE C3a and C5a Cytokines
110
what are prostaglandins and leukotrienes drerived from
Arachidonic acid
111
how are prostaglandins made from arachidonic acid
Cyclo-oxygenase
112
how are leukotrienes made from arachidonic acid
lipo-oxygenase
113
how does Asprin and non-steroidal anti-inflmmatory drugs reduce inflammmation
Blocking cyclo-oxygenase activity | - inhibit release of arachidonic acid from cell membrane phospholipids
114
what prostaglandins don;t cause vasodilation
thromboxane A2 (vasoconstriction)
115
action of thromboxane on platelet aggregation
Promotes platelet aggregation
116
action of prostacyclin on platelet aggregation
Inhibits platelet aggregation
117
what are the consequences of Injury
Regeneration or repair
118
what does regenetaion include
REnewing tissues | Stable tissues
119
what is renewing tissue
Complete regeneation after injury
120
what does renewing tissues when injured
Epidermis GI tract Epithelium hematopoietic system
121
what is regenration via stable tissues
Compensatory growth
122
what does Compensatory growth
Liver and kidney
123
what are possibilities of repair
Wound | Chronic inflammation
124
Would healing leads to what
Scar formation
125
chronic inflammation leads
Fibrosis
126
what cells are continuously dividing
Hematopoietic cels | Surface epithelium
127
what are stable cells
Minimal replicating in normal conditions, but can proliferate in response to injury
128
what cells are considered to be stable cells
Parenchymal cells of most solid organs Smooth muscle Fibroblasts
129
what are permanent cels
No capacity for proliferation
130
what are permanent cells in the body
Neurons | Cardiac muscle
131
steps of Healing by first(primary) intention
Blood clot (minutes) neutrophils (24 hours) Early proliferation/migration of epithelial cells (24-48 hours) Macrophages replace neutrophils; early granulation tissue (day 3) Peak neovascularization (Day5) Progressive collagen deposition (During 2nd week( Increased wound stregnth (next 4 months)
132
differnece between 1st and second healing by intention
Second has more inflammation, more granulation tissue | wound contraction due to myofibroblasts
133
what causes wound contaction in second intension
Mycofibroblasts
134
what factors affect wound healing
``` Infection Nutrition (protein and vitamins) Steroids Mech factors Poor perfusion - Diabetes mellitus -athreosclerosis ```
135
what is the number one cause of delayed healing
Infection

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