Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

605 Pathology > Acute Inflammation (Rosser) > Flashcards

Acute Inflammation (Rosser) Flashcards

1
Q

inflammation

A

the reaction of vascularized, living tissue to local injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 Major Goals of Inflammatory Reactions

A
  1. Eliminate the injurious stimulus
  2. Repair associated tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Five Cardinal Signs of Inflammation

A
  1. Redness
  2. Swelling
  3. Heat
  4. Pain
  5. Loss of Function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Can inflammation occur after death?

A

no - presence of inflammatory cells means something happened antemortem, not postmortem!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Variables in Inflammation

A

intensity, magnitude, duration

dependent on innate response, immunologic status of host, and the type of agent involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Benefits of Inflammation

A
  1. Degrade foreign materials
  2. Provide wound healing factors
  3. Dilution/inactivation of biological or chemical toxins
  4. Killing/sequestration [of microbes, necrotic tissue, neoplasia]
  5. Restrict movement to allow for healing and repair
  6. Increase temperature (local or systemic) to induce vasodilation and inhibit microbial replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

5 Main Phases of the Inflammatory Response

A
  1. Recognize inflammatory stimulus
  2. Acute vascular response
  3. Acute cellular response
  4. Chronic cellular response
  5. Resolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Exogenous Substances which Induce Tissue Injury

A
  1. Microbes
  2. Foreign Bodies
  3. Mechanical Action (traumatic injury)
  4. Physical Action (think burns, frostbite)
  5. Chemical Substances (think venoms, caustic agents)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Endogenous Substances Inducing Tissue Injury

A
  1. Autoimmune reactions
  2. Intracellular signals released from injured or dying cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PAMPs

A

pattern/pathogen-associated molecular patterns highly conserved microbial ligands (so unique to microbes) and binding triggers release of inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TLR-4

A

PRR which recognizes lipopolysaccharide (LPS) in gram-negative cell bacterial walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

TLR-3

A

PRR for double stranded RNA (viruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PRR

A

pattern recognition receptor located on host cells; binding of PAMPS from microbes to PRRs results in downstream induction of inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

DAMPs

A

Damage Associated molecular patterns
endogenous molecules released from damaged or dying cells within the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Difference between PAMPs and DAMPs?

A

PAMPs are from microbes and differentiate self from non-self
DAMPs are from the host and differentiate healthy self from damaged self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Examples of DAMP Mechanisms/Sources (3)

A
  1. extracellular presence of certain molecules
  2. intracellular enzymes–> breakdown of components
  3. circulating antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Do both PAMPS and DAMPs bind to PRRs?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What vasoactive mediators are contained in mast cells?

A

histamine and serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Histamine and Serotonin

A

released from mast cells at the site of injury to cause vasodilation and increased vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Resident Tissue Macrophages

A

also bind PRRs in response to inflammatory stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Epithelial Cells

A

can secrete cytokines when injured or recognize inflammatory stimuli via PRRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What activates platelets?

A

the exposure of subendothelial collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Inflammatory Mediators from Platelets

A

histamine and serotonin (like mast cells) but also complement activators, platelet activating factor, and coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

bradykinin

A

released from damaged vascular endothelium and causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
prostaglandins and leukotrienes
can come from many cell types in response to PRR activation; causes vasodilation and increased vascular permeability
26
platelet-activating factor (PAF)
can come from many cell types in response to PRR activation; causes increased vascular permeability and smooth muscle contraction
27
hyperemia
tissue redness d/t blood pooling
28
biphasic nature of vascular permeability response
Early Phase occurs immediately, rapid and short lived, in response to histamines (and kinins etc) Later phase is cytokine dependent (IL-1, TNFa, and kinins)
29
Net Effect of the Acute Vascular Response
increased capillary hydrostatic (push) pressure
30
Edema
leakage of plasma proteins
31
First cell to make it out of the vasculature in response to injury?
neutrophils
32
macrophages in the inflammatory response
larger number with a longer duration of infection (chronicity)
33
Eosinophils respond to what stimuli?
parasitic disease and acute hypersensitivity reaction
34
lymphocytes and plasma cells respond to what stimuli?
antigenic, or delayed HST
35
3 Granulocytes
1. Neutrophils 2. Eosinophils 3. Basophils
36
are granulocytes terminally differentiated?
yes (they are fully mature before leaving the bone marrow)
37
3 Steps of the Leukocyte Adhesion Cascade
1a. Rolling 1b. Adhesion/Pavementing 2. Migration 3. Chemotaxis
38
leukocyte adhesion cascade
how neutrophils move from vasculature into tissue
39
Rolling
blood flow slows, then neutrophil ligands (capital L goes with leukocytes) interact with selectins on the endothelial surface and will "roll along" before coming to an eventual stop
40
Pavementing/Adherence
final part of adhesion where after the leukocyte stops, it is flattened on the endothelial surface
41
Cytokines in Induction of Pavementing?
IL-1 and TNFa
42
Ligands on Surface of Neutrophils Involved in Adhesion
Sialyl Lewis and L-selectin
43
Ligands on Endothelium Involved in Adhesion
P-selectin and E-selectin
44
Ligands on Leukocyte involved in Pavementing
beta2 integrins (CD11/CD18)
45
Ligands on Endothelium involved in Pavementing
ICAM-1 and VCAM-1
46
diapedesis
actual passage of the leukocyte through wall of blood vessel
47
PECAM-1
ligand on both leukocyte and endothelium and binds to itself
48
Summary of Leukocyte Adhesion Cascade
49
Chemotaxis
migration of a leukocyte in response to chemotactic mediators (like IL-8)
50
pseudopedia
cytoplasm changes within the leukocyte that allows the cell to "ooze" towards the stimulus, with actin/myosin contracting behind to push through towards inciting agent
51
Heterophils in Rabbits/GPs/Elephants
function as neutrophils but appear with bright red granules on morphology
52
Heterophils in Birds and Reptiles
functionally different from neutrophils (lack myeloperoxidase) and have elongated red granules on morphology
53
Is phagocytosis receptor mediated?
yes - Fc receptors and Complement CR1 and CR3
54
opsonization
coat pathogen with plasma proteins (opsonins) to taget for phagocytosis
55
Can IgG and C3b directly recognize bacteria?
yes
56
respiratory burst steps
1. Lots of oxygen 2. Becomes superoxide anion, which is cytotoxic 3. superoxide anion can form hydrogen peroxide
57
respiratory burst
needed to effectively kill bacterial and fungal agents
58
Fenton Reaction
requires iron to generate a hydroxyl free radical
59
Are free radicals produced during respiratory burst specific to the antigen?
no - can cause collateral damage to healthy tissue
60
source of iron for Fenton reaction
lactoferrin in neutrophil granules
61
Myeloperoxidase
enzyme in neutrophils which converts hydrogen peroxide and chloride ions into hypochlorous acid (oxidizing agent) makes pus!
62
What species lack myeloperoxidase?
birds and reptiles they'll have more caseous/granulomatous inflammation
63
Neutrophil Extracellular Traps (NETs)
when neutrophils die, these are released and can physically entrap bacteria and can be microbicidal
64
2 Major Types of Degradative Neutrophil Granules
1. Specific 2. Azurophilic
65
specific granules
fuse with phagolysosome first and acidify the phagolysosomal compartment includes lysozyme and lactoferrin (iron)
66
azurophilic granules
fuse with phagolysosome later includes myeloperoxidase and also lysozyme
67
IL-8
the most specific chemotactic power for neutrophils; stimulates neutrophil production and release from bone marrow
68
proinflammatory cytokines
TNFa, IL-1, IL-12 (and more)
69
IL-5
chemotactic stimuli for eosinophils, and is SPECIFIC for eosinophils
70
Are eosinophils present in all lesions?
no, mainly parasitic and some immune mediated hypersensitivity reactions
71
Are eosinophils present in all tissues?
yes
72
Major Basic Protein (MBP)
most important component of eosinic granules which is parasiticidal
73
Push-Pull Relationship of Mast Cells and Eosinophils
Mast cells eat the MBP from the eosinophils and produces IL-5 to call more eosinophils in Eosinophils degrade components from the mast cell granules (including histamine, PAF, and heparin)
74
IL-5 is produced by what cells?
eosinophils, mast cells, and Th2 lymphocytes
75
Are NK cells seen cyto or histologically?
no
76
IL-21
main cytokine involved in NK cell function and differentiation
77
perforin
in the granules in NK cells (and CD8 T cells); destroy target cells by creating pores in their membranes
78
Monocytes become what cell type?
macrophages
79
2 Types of Macrophages
M1 and M2
80
Which type of macrophage is involved in the inflammatory response?
M1
81
M2 Macrophages
fixed tissue macrophages that hang out under normal physiologic conditions to perform housekeeping functions (like removing cells and debris from tissue remodeling)
82
Cool Summary with Pictures
83
3 types of inflammatory mediators
1. Preformed (histamine) 2. Synthesized (cytokines, PGs) 3. Plasma derivedF
84
Bradykinin
triggered from factor 12 of the coagulation cascade; is a slow-acting vasodilator and produces sustained redness, heat, and pain
85
What serves as the link between inflammation and coagulation?
kinins
86
Anaphylotoxins
C3a and C5a (increase vascular permeability and microbes destroyed by leukocytes)
87
C3b
opsonin to bind CR1 and 3 on neutrophils to cause phagocytosis of microbe
88
C5b
initiates formation of the membrane attack complex (MAC) resulting in lysis of the microbe
89
C5a
chemoattractant for leukocytes and increased vascular permeability
90
C3a and C5a
increase vascular permeability
91
Eicosanoids
synthesized mediators which are arachidonic acid metabolites from the COX and LOX pathways
92
prostaglandins and thromboxanes
prostaglandins cause vasodilation thromboxane A2 causes vasoconstriction
93
leukotrienes
LTC4, LTD4, LTE4 all increase capillary permeability
94
IL-1 and TNFa
fever, T cell and macrophage activation
95
IL-6
acute phase protein production
96
IL-10
suppresses macrophage function
97
Positive Acute Phase Proteins
tend to increase in concentration during inflammatory response C-reactive protein Serum Amyloid A Fibrinogen
98
Negative Acute Phase Proteins
tend to decrease in concentration during inflammatory response Albumin Transferrin

605 Pathology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions