Inflammation 1 Flashcards
1
Q
what is inflammation
A
an integrated and tightly controlled set of events associated with the body’s response to:
- injury
- infection
- insult
- itself
2
Q
injury
A
trauma
tissue damage/necrosis
3
Q
infection
A
bacterial
fungal
virus
4
Q
insult
A
chemical radiation thermal foreign body environmental substances
5
Q
itself
A
autoimmunity to self antigens
6
Q
cardinal signs of inflammation
A
external manifestations of vascular change and leukocyte recruitment/activation
7
Q
examples of the cardinal signs of inflammation
A
- Calor (heat)
- Rubor (redness)
- Tumor (swelling)
- Dolor (pain)
- Functio laesa (loss of function)
8
Q
what are the 5 R’s of inflammatory response
A
- Recognition of injurious agent
- Recruitment of leukocytes
- Removal of agent
- Regulation (control) of response
- Resolution (repair) of damaged tissue
9
Q
what happens if injury persists
A
chronic inflammation
10
Q
what is acute inflammation
A
immediate response (minutes to days)
11
Q
what is the specificity of acute inflammation
A
limited specificity
12
Q
characteristics of acute inflammation
A
- neutrophils
* fluid and plasma exudation
13
Q
chronic inflammation
A
delayed response (days to years)
14
Q
specificity of chronic inflammation
A
more specificity
15
Q
characteristics of chronic inflammation
A
- lymphocytes & plasma cells
- vascular proliferation and scarring
16
Q
vascular changes of acute inflammation
A
- vasodilation
- increased vascular permeability
17
Q
cellular events of acute inflammation
A
- neutrophil emigration
- cellular recruitment
- activation of neutrophils
18
Q
what is vasodilation
A
locally increased blood flow due to arteriolar smooth muscle relaxation
19
Q
vasodilation is mediated by what
A
prostaglandins
histamine
bradykinin
20
Q
characteristics of vasodilation
A
- erythema (rumor)
- warmth (calor)
21
Q
what occurs with increased vascular permeability
A
- movement of protein-rich fluid into extra-vascular space
- endothelial contraction (histamine)
- endothelial disruption (tissue damage)
- swelling (tumor)
22
Q
what is effusion
A
-greater than normal volume of fluid within the pericardial, abdominal or pulmonary cavity
23
Q
classifications of effusion
A
- transudate
- exudate
found in pleural or peritoneal cavity
24
Q
how do differentiate between transudate and exudate
A
-based primarily on the protein [ ]
25
transudates
fluids of non-inflammatory origin with low protein concentration
26
transudates caused by increased volume caused by alterations in hydrostatic factors as:
- increased venous pressure (heart failure, hepatic cirrhosis with portal hypertension)
- hypoproteinemia (nephrotic syndrome, protein losing enteropathy)
- lymphatic blockage
27
exudates characterized by
- increased protein concentration
- frequently contain inflammatory cells (turbid0
- glucose concentration decreased
28
exudates caused by
- malignancy
- infection
- pancreatitis
29
where can effusion be collected from
-chest or abdomen - semi surgical procedures
30
what is thoracentesis
- collection of effusion through chest wall
| - plural fluid
31
what is paracentesis
- through abdominal wall
| - ascitic fluid
32
what is pericardiocentesis
- collection of effusion from pericardium
- pericardial fluid
- not a bedside procedure
33
what are the mediators of acute inflammatory response
- neutrophils
- endothelial cells
- mast cells
- eosinophils
- platelets
- toll like receptors
- arachidonic acid metabolies
- complement
- Hageman factor (Factor XII)
34
where do mature neutrophils emerge from
bone marrow
35
neutrophils are controlled by
chemokines (can circulate in blood for 6-8 h in blood)
36
what are other clinical names of neutrophils
- polymorphonuclear cells
- PMNS
- polys
- segs
37
neutrophils are central to acute or chronic inflammation
acute
38
action of neutrophils
phagocytose microorganisms and tissue debris
39
appearance of neutrophils
cytoplasm with granules (primary, secondary, tertiary)
40
what do neutrophils express
-selectins and integrins for binding to other cells and to migrate out into interstitum
41
neutrophils express receptors which recognize
- Fc porton of IgG and IgM
- C5a, C3b and iC3b (complement)
- cytokines
42
how are neutrophil extracellular traps formed
when neutrophils undergo oxidative burst and degranulation
43
what are endothelial cells
monolayer of cells lining blood vessels
44
function of endothelial cells
- regulates vascular contraction and relaxation
| - regulates platelet aggregation
45
do nonactivated platelets bind normal endothelium
no
46
what can endothelial cells express
unregulated levels of adhesion molecules (ICAM and VCAM) which can anchor activated neutrophils
47
where are mast cells located
adjacent to vessels and widely distributed throughout connective tissue (ie. lug, GI mucosal surfaces, skin)
48
what do mast cells contain
preformed histamine granules (aretriolar vasodilation and increased vascular permeability of postcapillary venues)
49
mast cells are activated by
-trauma
-cross-linking of cell-surface IgE receptors
C3a and C5a complement proteins
50
what is the immediate response of mast cells
release of preformed histamine granules
51
what is the delayed response of mast cells
- arachidonic acid metabolites (leukotrienes)
| - second phase of mast cell acute inflammatory response)
52
soon after the release of mast cells it is inactivated by
histaminase
53
eosinophils are associated with what type of reaction
- allergic rxn
- parasite associated rxn
- acute and chronic inflammatory rxns
54
eosinophils release
-cytoplasmic granules with lysosomal enzymes, cytokines and major basic protein (toxic to parasites)
55
platelets are formed from
megakaryocytes in bone marrow
56
appearance of platelets
bits of cytoplasm (no nucleus)
57
platelets contain
inflammatory mediators as dense granules and alpha granules
58
function of platelets
promote clot formation
59
toll-like receptors are present on what type of cells
- innate immune system (macrophages, dendritic cells)
- epithelial cells
- lymphocytes
60
function of toll-like receptors
recognize molecular structures common to microbes
61
TLR activation leads to upregulation of
cytokines
62
arachidonic acid is released from
phospholipid cell membrane by phopholipases
63
what are arachidonic acid metabolites called
eicosanoids
64
arachidonic acid derived from
20 carbon F/As
65
what are the 2 main pathways of arachidonic acid
- cyclooxygenase produces prostaglandins
| - 5-lipoxygenase produces leukotrienes
66
what factors ofthe cyclooxygenase pathway cause vasodilation and increased vascular permeability
PGI2
PGD2
PGE2
67
what mediates pain in the cyclooxygenase pathway
PGE2
68
what causes vasoconstriction and platelet aggregation in the cyclooxygenase pathway
TXA2
69
what causes neutrophil chemotaxis and activation in the 5-lipoxygenase
LTB4
70
what causes smooth muscle contraction (vasoconstriction, brochospasm, increased vascular permeability)
LTC4
LTD4
LTE4
71
what causes neutrophil inhibition in 5-lipoxygenase
LXA4
| LXB4
72
what is complement
serum proteins which "complement"/help host defense and inflammation
73
complement proteins C1 to C9 circulate as
inactive precursors
74
what is the critical step of complement
formation of C3 convertase which cleaves and activates C3
75
C3 cleavage occurs in what 3 pathways
1. alternative pathway
2. classical pathway
3. lectin pathway
76
classical pathway
C1 complement component binds IgG or IgM bound to antigen
77
alternative pathway
microbial cell wall components (ie. endotoxin) directly activates complement
78
lectin pathway
plasma lectin binds to mannose residues on microbes (direct pathway)
79
what are the complement disorders
1. hereditary angioedema
2. paroxysmal nocturnal hemoglobinuria (PNH)
3. Factor H deficiency
80
what is Hereditary angioedema
-deficiency of C1 inhibitor
81
function of C1 inhibitor
regulator of various components of clotting, complement and clotting cascade
82
consequences of hereditary angioedema
- increased vascular permeability under skin
- submucosal and subcutaneous swelling
- laryngeal edema can lead to death
83
what is paroxysmal nocturnal hemoglobinuria (PNH)
-deficiency of decay activating factor (DAF)
84
function of DAF (decay activating factor)
normally limits C3 and C5 formation
85
PNH results in
complement-mediated lysis of RBCs (Hemolytic anemia)
86
function of factor H
normally limits convertase formation
87
Factor H deficiency results in
- higher than normal C3b deposition on endothelium
- hemolytic uremia syndrome (HUS)
- spontaneous vascular permeability in macular degeneration of eye
88
what is the product of the kinin system
bradykinin
89
what are the direct effects of bradykinin
- increased vascular permeability (very potent)
- arteriolar dilatation
- pain
90
bradykinin is inactivated by
kininases in plasma and tissue
